Journal: bioRxiv

Article Title: Polo-like kinase 1 controls activation of adult neural stem cells and represents a druggable entry-point to boost adult neurogenesis

doi: 10.64898/2026.05.12.724486

Figure Lengend Snippet: (A) Expression of Plk1 in SEZ populations. Principal component analysis (PCA) of bulk RNA-seq profiles from SEZ cell populations and their biological replicates ( Belenguer et al ., 2021 ). The first two components account for 62.2% of the total variance, with samples and labels colored by log-normalized Plk1 expression. qNSC, quiescent NSC; pNSC, primed-to-activate NSC; aNSC, active NSC; NPC1 and 2, neural progenitor cell populations 1 and 2; NB1 and 2, neuroblast population 1 and 2. Dataset GEO: GSE138243 . (B) Schematic depicting the BrdU injection-chase protocol used in Plk1 Gfap(+/+) and Plk1 Gfap(+/ Δ) mice. (C) Confocal micrographs of the staining for BrdU + -retaining cells (gray, yellow arrowheads) in the SEZ (delimited by white dashed lines) of Plk1 Gfap(+/+) and Plk1 Gfap(+/ Δ) mice. Nuclei are stained with DAPI (blue). Scales: 20 μm and 10 μm (insets). ( D ) Quantification of the percentage of BrdU + cells in the SEZ of Plk1 Gfap(+/+) (N = 6) and Plk1 Gfap(+/ Δ) (N = 4) relative to the total number of cells. ( E ) Confocal micrographs of the SEZ Plk1 Gfap(+/+) and Plk1 Gfap(+/Δ) mice, immunostained for the neuroblast marker DCX (gray). Nuclei are stained with DAPI (blue). Scale bars: 20 μm. Dashed white lines delimit the boundaries of the SEZ. ( F ) Quantification of the percentage of DCX + cells in the SEZ of Plk1 Gfap(+/+) (N = 5) and Plk1 Gfap(+/ Δ) (N = 5) mice. (G) Schematic depicting the CldU and BI 6727 injection-chase protocol used in wild-type mice. ( H ) Confocal micrographs of the SEZ (white dashed lines) of control or BI 6727-treated mice immunostained for CldU (gray, yellow arrowheads). Full yellow arrowheads point at CldU high cells. Cell nuclei are stained with DAPI (blue). Scale bars: 20 μm. LV, lateral ventricle. ( I ) Quantification of the percentage of CldU + cells in the SEZ of vehicle-(control, N = 5) or BI 6727-treated mice (N = 4). ( J ) Percentage of high intensity CldU + (CldU high ) within the total of CldU + cells in the SEZ of vehicle- (control, N = 5) or BI 6727-treated mice (N = 4). ( K ) Example confocal micrographs of the co-staining for BrdU (gray) and the proliferation marker Ki67 (green) in a BI 6727-treated wild-type mouse. The white dashed lines delimit the SEZ. The white, full arrowhead points at a BrdU + -Ki67 - cell, the green arrowheads point at a BrdU - -Ki67 + cells, and one activated NSC is identified as BrdU + -Ki67 + double positive cell (yellow, full arrowhead). Scale bars: 20 μm. ( L ) Percentage of cycling (Ki67 + )-high intensity CldU + (CldU high ) cells in the SEZ of vehicle- (control, N = 5) or BI 6727-treated mice (N = 4). Data are represented as box and whiskers from min. to max and all data points are shown. * p < 0.05 by two-tailed unpaired Student ’s t -tests ( D, F, I, J ) and Mann-Whitney ’s test ( L ). Symbols represent biological replicates ( A ) or mean data from individual mice ( D, F, I, J, L ).

Article Snippet: To conditionally inactivate Plk1 in NSCs, male Plk1 (lox/lox) mice were crossed with females expressing Cre recombinase downstream of the murine glial fibrillary acidic protein ( Gfap ) promoter, obtained from Jackson Laboratories (Tg(Gfap-cre)73.12Mvs/J) ( Garcia et al ., 2004 ), to generate Plk1 (+/lox) ;Gfap (+/Cre) mice, and are referred herein to as Plk1 Gfap(+/ Δ) .

Techniques: Expressing, RNA Sequencing, Injection, Staining, Marker, Control, Two Tailed Test, MANN-WHITNEY

Journal: bioRxiv

Article Title: Polo-like kinase 1 controls activation of adult neural stem cells and represents a druggable entry-point to boost adult neurogenesis

doi: 10.64898/2026.05.12.724486

Figure Lengend Snippet: (A) Representative PCR for the Plk1 -floxed recombined allele in brain tissue sections from Plk1 Gfap(+/+) and Plk1 Gfap(+/Δ) mice. ( B ), Percentage of Ki67 + cells in the SEZ of vehicle (control, N = 3) and BI 6727-treated (N = 3) mice. (C) , Representative confocal micrographs for Ki67 (gray) in BI 6727-treated mice. Scale bars: 50 μm, and 20 μm (inset). The white dashed lines delimit the boundary between the lateral ventricle (LV) and the subependymal zone (SEZ). Cell nuclei were labelled with DAPI (blue). Data are represented as box and whiskers from min. to max and all data points are shown. **p < 0.01, unpaired two tailed Student’s t test. Each symbol represents the mean value from an individual mouse (N).

Article Snippet: To conditionally inactivate Plk1 in NSCs, male Plk1 (lox/lox) mice were crossed with females expressing Cre recombinase downstream of the murine glial fibrillary acidic protein ( Gfap ) promoter, obtained from Jackson Laboratories (Tg(Gfap-cre)73.12Mvs/J) ( Garcia et al ., 2004 ), to generate Plk1 (+/lox) ;Gfap (+/Cre) mice, and are referred herein to as Plk1 Gfap(+/ Δ) .

Techniques: Control, Two Tailed Test

Journal: bioRxiv

Article Title: Polo-like kinase 1 controls activation of adult neural stem cells and represents a druggable entry-point to boost adult neurogenesis

doi: 10.64898/2026.05.12.724486

Figure Lengend Snippet: (A) Quantification of the number of neurospheres obtained from freshly disaggregated SEZ tissue from Plk1 (+/lox) mice, treated with vehicle- (N = 4) and 4-OH-tamoxifen (Tam) (N = 4). Data are represented as box and whiskers from min. to max and all data points are shown. * p < 0.05, by Mann-Whitney ’s test. Dots represent independent cell cultures. ( B ) Western blot for Plk1 and β-actin as loading control in lysates from control or Tam-treated neurospheres from Plk1 (+/lox) mice. (C) Schematic depicting the pipeline followed in the label-free differential analysis of phosphoproteins by liquid chromatography coupled with tandem mass spectrometry performed in Plk1 (+/lox) vehicle-(N = 4) and Tam-treated (N = 4) neurospheres ( D ) Identified phosphorylation distribution by residue type. ( E ) Volcano plot showing all phosphopeptides identified in ≥ 2 replicates. Blue lines and background indicate the sector of the plot that include the cut-off values ( q value = 0.05, and Log2 [Tam/Vehicle] = ± 1.0). Yellow dots indicate known Plk1-dependent (indicated in yellow boxes) or Plk1-inhibitor-sensitive phosphosites (in white boxes). In every case the position of the residue corresponds to the mouse protein. ( F, G ) Over-representation analysis network representation of the 40 most differentially regulated genes found in Tam-treated NSCs vs . control. Gene ontologies (GO)-cellular component ( F ) and biological processes ( G ) are shown. Similar gene sets are grouped into functional modules. The node size represents the number of genes, the node colour correlates with the FDR q-value, and the edge width with the number of overlapping genes. ( H ) Venn diagram showing the genes from this study common to a list of PLK1 interactors (BioGRID). ( I ) KEGG pathway analysis of the list of 120 common genes, showing ‘Ubiquitin mediated proteolysis’ as the top pathway represented, and the gene names corresponding to each category. ( J ) Immunoprecipitation (IP) of HUWE1 showing co-IP with PLK1 in representative immunoblots (IB) for the specific detection of HUWE1 and PLK1 in lysates from transfected HEK293T cells. IgG, isotype control antibody. One experiment is shown out of three performed with similar results. Irrelevant lanes were cropped out of the image (dashed black lines). For full Western blot images refer to .

Article Snippet: To conditionally inactivate Plk1 in NSCs, male Plk1 (lox/lox) mice were crossed with females expressing Cre recombinase downstream of the murine glial fibrillary acidic protein ( Gfap ) promoter, obtained from Jackson Laboratories (Tg(Gfap-cre)73.12Mvs/J) ( Garcia et al ., 2004 ), to generate Plk1 (+/lox) ;Gfap (+/Cre) mice, and are referred herein to as Plk1 Gfap(+/ Δ) .

Techniques: MANN-WHITNEY, Western Blot, Control, Liquid Chromatography, Mass Spectrometry, Phospho-proteomics, Residue, Functional Assay, Ubiquitin Proteomics, Immunoprecipitation, Co-Immunoprecipitation Assay, Transfection

Journal: bioRxiv

Article Title: Polo-like kinase 1 controls activation of adult neural stem cells and represents a druggable entry-point to boost adult neurogenesis

doi: 10.64898/2026.05.12.724486

Figure Lengend Snippet: (A) Representative Western blots in lysates obtained from cultures of Plk1 (+/Ki) NSCs treated with increasing doses of doxycycline (Dox) to induce the expression of a FLAG-tagged human PLK1 transgene. Samples were run in parallel and detected with anti-FLAG or Plk1, and β-actin antibodies for loading control. ( B ) Quantification of the number of primary neurospheres obtained from Plk1 (+/Ki) NSCs in the absence or presence of Dox. Values were normalized to vehicle-treated cells. N = 3 for both conditions. Data are represented as box and whiskers from min. to max and all data points are shown. *** p < 0.001, two-tailed paired Student’s t -tests. Each symbol represents one independent neurosphere culture obtained from different mice (N).

Article Snippet: To conditionally inactivate Plk1 in NSCs, male Plk1 (lox/lox) mice were crossed with females expressing Cre recombinase downstream of the murine glial fibrillary acidic protein ( Gfap ) promoter, obtained from Jackson Laboratories (Tg(Gfap-cre)73.12Mvs/J) ( Garcia et al ., 2004 ), to generate Plk1 (+/lox) ;Gfap (+/Cre) mice, and are referred herein to as Plk1 Gfap(+/ Δ) .

Techniques: Western Blot, Expressing, Control, Two Tailed Test

Journal: bioRxiv

Article Title: Polo-like kinase 1 controls activation of adult neural stem cells and represents a druggable entry-point to boost adult neurogenesis

doi: 10.64898/2026.05.12.724486

Figure Lengend Snippet: (A) Venn diagram indicating the number of proteins in this study common with studies of and . ( B ) List of 50 common proteins to the three studies. ( C ) HUWE1 phosphopeptides found in our study showing the modified residue (yellow). Blue box denotes that the phosphopeptide was differentially regulated (q < 0.05), whereas gray boxes denote a putative regulation (q > 0.05) in Plk1 (+/Δ) NSCs.

Article Snippet: To conditionally inactivate Plk1 in NSCs, male Plk1 (lox/lox) mice were crossed with females expressing Cre recombinase downstream of the murine glial fibrillary acidic protein ( Gfap ) promoter, obtained from Jackson Laboratories (Tg(Gfap-cre)73.12Mvs/J) ( Garcia et al ., 2004 ), to generate Plk1 (+/lox) ;Gfap (+/Cre) mice, and are referred herein to as Plk1 Gfap(+/ Δ) .

Techniques: Modification, Residue, Phospho-proteomics

Journal: bioRxiv

Article Title: Polo-like kinase 1 controls activation of adult neural stem cells and represents a druggable entry-point to boost adult neurogenesis

doi: 10.64898/2026.05.12.724486

Figure Lengend Snippet: ( A ) Representative immunoblot of Ascl1 and α-tubulin (loading control) in lysates from wild-type NSC-cultures treated with vehicle (DMSO) or the Plk1 inhibitors BI 2536 (left) and BI 6727 (right) at 5 and 7.5 nM. ( B ) Levels of Ascl1 normalized to loading control (α-tubulin) in control (DMSO) and BI 2536 (left) and BI 6727 (right)-treated wild type NSC protein extracts, represented in arbitrary units (a.u.) (N = 3, for each condition). ( C ) Representative immunoblots for Plk1, Ascl1, Cyclin D1, Cyclin D2 and Gapdh or β-actin for loading controls in Plk1 (+/lox) and Plk1 (+/K i ) NSCs in the absence or presence of 4-OH-tamoxifen (Tam) and Doxycycline (Dox), respectively. ( D) Levels of Ascl1 in extracts from Plk1 (+/lox) NSCs in the presence of vehicle (-) or Tam, and Plk1 (+/K i ) NSCs in the presence of vehicle (-) or Dox, represented in arbitrary units (a.u.) after normalisation to the loading control (N = 6, Plk1 (+/lox) ; N = 3, Plk1 (+/K i ) in both treatment conditions, respectively). ( E ) Levels of Cyclin D2 normalised to the loading control in extracts from Plk1 (+/lox) NSCs in the presence of vehicle (-) or Tam (N = 3, in both treatment conditions), and Plk1 (+/K i ) NSCs in the presence of vehicle (-) or Dox (N = 5, in both treatment conditions), represented in arbitrary units (a.u.). ( F ) Representative immunoblots of the protein levels of PLK1-cerulean, Ascl1-myc and VINCULIN (loading control) in lysates obtained from HEK293T cells co-transfected with myc -tagged Ascl1 and either wild type human version of PLK1-cerulean (PLK1 WT -cer), its kinase-dead mutant (PLK1 K82R -cer) or a constitutively active mutant (PLK1 T210D -cer). Cells co-transfected with an empty vector (vector) and untransfected cells (-) were used as controls. The asterisk indicates a non-specific band detected by the Plk1 antibody at 110 kDa. ( G ) Densitometric quantification of Ascl1- myc normalised to loading controls and expressed as arbitrary units (a.u.) in HEK293T cells co-transfected with Ascl1- myc and either PLK1 WT -cer or mutants PLK1 K82R -cer or PLK1 T210D -cer. N = 7 independent transfections for each condition. ( H ) Representative confocal images of the immunodetection of Ascl1- myc (gray) in transfected HeLa cells in mitosis (yellow dashed lines) treated with MG-132, the Plk1 inhibitor BI 6727 or HUWE1 inhibitor BI 8626. Note the typical monopolar spindle-morphology provoked by the full inhibition of PLK1. ( I ) Mean fluorescence intensity (MFI) of Ascl1- myc in mitotic HeLa cells (n) treated with the different inhibitors (n = 74, 77, 70 and 67 independent cells, respectively) in N = 4 independent transfection experiments. ( J ) HUWE1 immunoprecipitation in HEK293T cells transfected with the indicated constructs, arrested in mitosis with nocodazole and treated with MG-132. A representative experiment showing interaction of HUWE1 with Plk1 and with Ascl1 is shown, out of three performed with similar results. Irrelevant lanes have been cropped out of the image (dashed black lines). ( K ) Representative immunoblots of PLK1-cerulean, PLK1 and Ascl1- myc protein levels obtained from untreated or MG-132-treated HEK293T cells co-transfected with myc -tagged Ascl1 and either wild type PLK1-cerulean or its mutant versions. Cells co-transfected with an empty vector (vector) and untransfected (-) cells were used as controls. Alpha-TUBULIN levels are shown as loading control and β-CATENIN and higher molecular weight ubiquitylated forms are shown as control for proteasome inhibition. ( L ) Levels of Ascl1- myc normalised to the loading control represented in arbitrary units (a.u.), in extracts from untreated or MG-132-treated HEK293T cells, co-transfected with Ascl1-myc and either the wild type or mutant versions of PLK1 . N = 6 for each condition. ( M ) Confocal micrographs of the staining for Ascl1 (gray) in control or BI 6727-treated wild-type mice. Cell nuclei were labelled with DAPI (blue). The white dashed lines delimit the SEZ. LV, lateral ventricle. Single channel images and insets (delimited by yellow dashed lines) for the staining of Ascl1 (right panels, gray, yellow arrowheads point at positive cells). Scale bars: 20 µm; inset: 10 µm. ( N ) Quantification of the percentage of Ascl1 + cells in the SEZ of control (N = 4) or BI 6727-treated (N = 4) wild-type mice. ( O ) Normalized mean fluorescence intensity (MFI) of Ascl1 per cell (n) in the SEZ of vehicle- (control; n = 318) or BI 6727-treated (n = 306) mice (N; N = 4 each). *P< 0.05, **p< 0.01 and ***p < 0.001, one-way ANOVA with Dunnett’s multiple comparison test ( B, G, I ), two-tailed unpaired Student’s t -tests ( D, E, N ), two-way ANOVA followed by Šidák’s multiple comparisons test ( L ) and Mann-Whitney’s test ( O ). Data are represented as box and whiskers from min. to max and all data points are shown ( B , D, E, G, L N and O ). Symbols represent mean values from independent neurosphere cultures obtained from individual mice ( B , D, E ), independent transfection experiments ( G, L ), independent mice ( N ) or individual cells ( O ). In ( I ) small symbols represent individual cells ( n ), and bigger symbols represent the mean values of each independent transfection experiment ( N ) and combined in a superplot representation. For full Western blot images refer to .

Article Snippet: To conditionally inactivate Plk1 in NSCs, male Plk1 (lox/lox) mice were crossed with females expressing Cre recombinase downstream of the murine glial fibrillary acidic protein ( Gfap ) promoter, obtained from Jackson Laboratories (Tg(Gfap-cre)73.12Mvs/J) ( Garcia et al ., 2004 ), to generate Plk1 (+/lox) ;Gfap (+/Cre) mice, and are referred herein to as Plk1 Gfap(+/ Δ) .

Techniques: Western Blot, Control, Transfection, Mutagenesis, Plasmid Preparation, Immunodetection, Inhibition, Fluorescence, Immunoprecipitation, Construct, Molecular Weight, Staining, Comparison, Two Tailed Test

Journal: bioRxiv

Article Title: Polo-like kinase 1 controls activation of adult neural stem cells and represents a druggable entry-point to boost adult neurogenesis

doi: 10.64898/2026.05.12.724486

Figure Lengend Snippet: Immunoprecipitation (IP) of PLK1 and Myc, showing the reciprocal interaction between Ascl1 and PLK1, and their interaction with HUWE1 in mitosis HEW293T cells. Representative immunoblots (IB) for the specific detection of HUWE1, PLK1 and Ascl1- myc in samples immunoprecipitated for PLK1 and Myc in lysates from transfected cells. IgG, isotype control antibody. One representative experiment out of three performed with similar results is shown.

Article Snippet: To conditionally inactivate Plk1 in NSCs, male Plk1 (lox/lox) mice were crossed with females expressing Cre recombinase downstream of the murine glial fibrillary acidic protein ( Gfap ) promoter, obtained from Jackson Laboratories (Tg(Gfap-cre)73.12Mvs/J) ( Garcia et al ., 2004 ), to generate Plk1 (+/lox) ;Gfap (+/Cre) mice, and are referred herein to as Plk1 Gfap(+/ Δ) .

Techniques: Immunoprecipitation, Western Blot, Transfection, Control

Journal: bioRxiv

Article Title: Polo-like kinase 1 controls activation of adult neural stem cells and represents a druggable entry-point to boost adult neurogenesis

doi: 10.64898/2026.05.12.724486

Figure Lengend Snippet: (A) Expression of Plk1 in SEZ populations. Principal component analysis (PCA) of bulk RNA-seq profiles from SEZ cell populations and their biological replicates ( Belenguer et al ., 2021 ). The first two components account for 62.2% of the total variance, with samples and labels colored by log-normalized Plk1 expression. qNSC, quiescent NSC; pNSC, primed-to-activate NSC; aNSC, active NSC; NPC1 and 2, neural progenitor cell populations 1 and 2; NB1 and 2, neuroblast population 1 and 2. Dataset GEO: GSE138243 . (B) Schematic depicting the BrdU injection-chase protocol used in Plk1 Gfap(+/+) and Plk1 Gfap(+/ Δ) mice. (C) Confocal micrographs of the staining for BrdU + -retaining cells (gray, yellow arrowheads) in the SEZ (delimited by white dashed lines) of Plk1 Gfap(+/+) and Plk1 Gfap(+/ Δ) mice. Nuclei are stained with DAPI (blue). Scales: 20 μm and 10 μm (insets). ( D ) Quantification of the percentage of BrdU + cells in the SEZ of Plk1 Gfap(+/+) (N = 6) and Plk1 Gfap(+/ Δ) (N = 4) relative to the total number of cells. ( E ) Confocal micrographs of the SEZ Plk1 Gfap(+/+) and Plk1 Gfap(+/Δ) mice, immunostained for the neuroblast marker DCX (gray). Nuclei are stained with DAPI (blue). Scale bars: 20 μm. Dashed white lines delimit the boundaries of the SEZ. ( F ) Quantification of the percentage of DCX + cells in the SEZ of Plk1 Gfap(+/+) (N = 5) and Plk1 Gfap(+/ Δ) (N = 5) mice. (G) Schematic depicting the CldU and BI 6727 injection-chase protocol used in wild-type mice. ( H ) Confocal micrographs of the SEZ (white dashed lines) of control or BI 6727-treated mice immunostained for CldU (gray, yellow arrowheads). Full yellow arrowheads point at CldU high cells. Cell nuclei are stained with DAPI (blue). Scale bars: 20 μm. LV, lateral ventricle. ( I ) Quantification of the percentage of CldU + cells in the SEZ of vehicle-(control, N = 5) or BI 6727-treated mice (N = 4). ( J ) Percentage of high intensity CldU + (CldU high ) within the total of CldU + cells in the SEZ of vehicle- (control, N = 5) or BI 6727-treated mice (N = 4). ( K ) Example confocal micrographs of the co-staining for BrdU (gray) and the proliferation marker Ki67 (green) in a BI 6727-treated wild-type mouse. The white dashed lines delimit the SEZ. The white, full arrowhead points at a BrdU + -Ki67 - cell, the green arrowheads point at a BrdU - -Ki67 + cells, and one activated NSC is identified as BrdU + -Ki67 + double positive cell (yellow, full arrowhead). Scale bars: 20 μm. ( L ) Percentage of cycling (Ki67 + )-high intensity CldU + (CldU high ) cells in the SEZ of vehicle- (control, N = 5) or BI 6727-treated mice (N = 4). Data are represented as box and whiskers from min. to max and all data points are shown. * p < 0.05 by two-tailed unpaired Student ’s t -tests ( D, F, I, J ) and Mann-Whitney ’s test ( L ). Symbols represent biological replicates ( A ) or mean data from individual mice ( D, F, I, J, L ).

Article Snippet: To conditionally inactivate Plk1 in NSCs, male Plk1 (lox/lox) mice were crossed with females expressing Cre recombinase downstream of the murine glial fibrillary acidic protein ( Gfap ) promoter, obtained from Jackson Laboratories (Tg(Gfap-cre)73.12Mvs/J) ( Garcia et al ., 2004 ), to generate Plk1 (+/lox) ;Gfap (+/Cre) mice, and are referred herein to as Plk1 Gfap(+/ Δ) .

Techniques: Expressing, RNA Sequencing, Injection, Staining, Marker, Control, Two Tailed Test, MANN-WHITNEY

Journal: bioRxiv

Article Title: Polo-like kinase 1 controls activation of adult neural stem cells and represents a druggable entry-point to boost adult neurogenesis

doi: 10.64898/2026.05.12.724486

Figure Lengend Snippet: (A) Representative PCR for the Plk1 -floxed recombined allele in brain tissue sections from Plk1 Gfap(+/+) and Plk1 Gfap(+/Δ) mice. ( B ), Percentage of Ki67 + cells in the SEZ of vehicle (control, N = 3) and BI 6727-treated (N = 3) mice. (C) , Representative confocal micrographs for Ki67 (gray) in BI 6727-treated mice. Scale bars: 50 μm, and 20 μm (inset). The white dashed lines delimit the boundary between the lateral ventricle (LV) and the subependymal zone (SEZ). Cell nuclei were labelled with DAPI (blue). Data are represented as box and whiskers from min. to max and all data points are shown. **p < 0.01, unpaired two tailed Student’s t test. Each symbol represents the mean value from an individual mouse (N).

Article Snippet: To conditionally inactivate Plk1 in NSCs, male Plk1 (lox/lox) mice were crossed with females expressing Cre recombinase downstream of the murine glial fibrillary acidic protein ( Gfap ) promoter, obtained from Jackson Laboratories (Tg(Gfap-cre)73.12Mvs/J) ( Garcia et al ., 2004 ), to generate Plk1 (+/lox) ;Gfap (+/Cre) mice, and are referred herein to as Plk1 Gfap(+/ Δ) .

Techniques: Control, Two Tailed Test

Journal: bioRxiv

Article Title: Polo-like kinase 1 controls activation of adult neural stem cells and represents a druggable entry-point to boost adult neurogenesis

doi: 10.64898/2026.05.12.724486

Figure Lengend Snippet: (A) Quantification of the number of neurospheres obtained from freshly disaggregated SEZ tissue from Plk1 (+/lox) mice, treated with vehicle- (N = 4) and 4-OH-tamoxifen (Tam) (N = 4). Data are represented as box and whiskers from min. to max and all data points are shown. * p < 0.05, by Mann-Whitney ’s test. Dots represent independent cell cultures. ( B ) Western blot for Plk1 and β-actin as loading control in lysates from control or Tam-treated neurospheres from Plk1 (+/lox) mice. (C) Schematic depicting the pipeline followed in the label-free differential analysis of phosphoproteins by liquid chromatography coupled with tandem mass spectrometry performed in Plk1 (+/lox) vehicle-(N = 4) and Tam-treated (N = 4) neurospheres ( D ) Identified phosphorylation distribution by residue type. ( E ) Volcano plot showing all phosphopeptides identified in ≥ 2 replicates. Blue lines and background indicate the sector of the plot that include the cut-off values ( q value = 0.05, and Log2 [Tam/Vehicle] = ± 1.0). Yellow dots indicate known Plk1-dependent (indicated in yellow boxes) or Plk1-inhibitor-sensitive phosphosites (in white boxes). In every case the position of the residue corresponds to the mouse protein. ( F, G ) Over-representation analysis network representation of the 40 most differentially regulated genes found in Tam-treated NSCs vs . control. Gene ontologies (GO)-cellular component ( F ) and biological processes ( G ) are shown. Similar gene sets are grouped into functional modules. The node size represents the number of genes, the node colour correlates with the FDR q-value, and the edge width with the number of overlapping genes. ( H ) Venn diagram showing the genes from this study common to a list of PLK1 interactors (BioGRID). ( I ) KEGG pathway analysis of the list of 120 common genes, showing ‘Ubiquitin mediated proteolysis’ as the top pathway represented, and the gene names corresponding to each category. ( J ) Immunoprecipitation (IP) of HUWE1 showing co-IP with PLK1 in representative immunoblots (IB) for the specific detection of HUWE1 and PLK1 in lysates from transfected HEK293T cells. IgG, isotype control antibody. One experiment is shown out of three performed with similar results. Irrelevant lanes were cropped out of the image (dashed black lines). For full Western blot images refer to .

Article Snippet: To conditionally inactivate Plk1 in NSCs, male Plk1 (lox/lox) mice were crossed with females expressing Cre recombinase downstream of the murine glial fibrillary acidic protein ( Gfap ) promoter, obtained from Jackson Laboratories (Tg(Gfap-cre)73.12Mvs/J) ( Garcia et al ., 2004 ), to generate Plk1 (+/lox) ;Gfap (+/Cre) mice, and are referred herein to as Plk1 Gfap(+/ Δ) .

Techniques: MANN-WHITNEY, Western Blot, Control, Liquid Chromatography, Mass Spectrometry, Phospho-proteomics, Residue, Functional Assay, Ubiquitin Proteomics, Immunoprecipitation, Co-Immunoprecipitation Assay, Transfection

Journal: bioRxiv

Article Title: Polo-like kinase 1 controls activation of adult neural stem cells and represents a druggable entry-point to boost adult neurogenesis

doi: 10.64898/2026.05.12.724486

Figure Lengend Snippet: (A) Representative Western blots in lysates obtained from cultures of Plk1 (+/Ki) NSCs treated with increasing doses of doxycycline (Dox) to induce the expression of a FLAG-tagged human PLK1 transgene. Samples were run in parallel and detected with anti-FLAG or Plk1, and β-actin antibodies for loading control. ( B ) Quantification of the number of primary neurospheres obtained from Plk1 (+/Ki) NSCs in the absence or presence of Dox. Values were normalized to vehicle-treated cells. N = 3 for both conditions. Data are represented as box and whiskers from min. to max and all data points are shown. *** p < 0.001, two-tailed paired Student’s t -tests. Each symbol represents one independent neurosphere culture obtained from different mice (N).

Article Snippet: To conditionally inactivate Plk1 in NSCs, male Plk1 (lox/lox) mice were crossed with females expressing Cre recombinase downstream of the murine glial fibrillary acidic protein ( Gfap ) promoter, obtained from Jackson Laboratories (Tg(Gfap-cre)73.12Mvs/J) ( Garcia et al ., 2004 ), to generate Plk1 (+/lox) ;Gfap (+/Cre) mice, and are referred herein to as Plk1 Gfap(+/ Δ) .

Techniques: Western Blot, Expressing, Control, Two Tailed Test

Journal: bioRxiv

Article Title: Polo-like kinase 1 controls activation of adult neural stem cells and represents a druggable entry-point to boost adult neurogenesis

doi: 10.64898/2026.05.12.724486

Figure Lengend Snippet: (A) Venn diagram indicating the number of proteins in this study common with studies of and . ( B ) List of 50 common proteins to the three studies. ( C ) HUWE1 phosphopeptides found in our study showing the modified residue (yellow). Blue box denotes that the phosphopeptide was differentially regulated (q < 0.05), whereas gray boxes denote a putative regulation (q > 0.05) in Plk1 (+/Δ) NSCs.

Article Snippet: To conditionally inactivate Plk1 in NSCs, male Plk1 (lox/lox) mice were crossed with females expressing Cre recombinase downstream of the murine glial fibrillary acidic protein ( Gfap ) promoter, obtained from Jackson Laboratories (Tg(Gfap-cre)73.12Mvs/J) ( Garcia et al ., 2004 ), to generate Plk1 (+/lox) ;Gfap (+/Cre) mice, and are referred herein to as Plk1 Gfap(+/ Δ) .

Techniques: Modification, Residue, Phospho-proteomics

Journal: bioRxiv

Article Title: Polo-like kinase 1 controls activation of adult neural stem cells and represents a druggable entry-point to boost adult neurogenesis

doi: 10.64898/2026.05.12.724486

Figure Lengend Snippet: ( A ) Representative immunoblot of Ascl1 and α-tubulin (loading control) in lysates from wild-type NSC-cultures treated with vehicle (DMSO) or the Plk1 inhibitors BI 2536 (left) and BI 6727 (right) at 5 and 7.5 nM. ( B ) Levels of Ascl1 normalized to loading control (α-tubulin) in control (DMSO) and BI 2536 (left) and BI 6727 (right)-treated wild type NSC protein extracts, represented in arbitrary units (a.u.) (N = 3, for each condition). ( C ) Representative immunoblots for Plk1, Ascl1, Cyclin D1, Cyclin D2 and Gapdh or β-actin for loading controls in Plk1 (+/lox) and Plk1 (+/K i ) NSCs in the absence or presence of 4-OH-tamoxifen (Tam) and Doxycycline (Dox), respectively. ( D) Levels of Ascl1 in extracts from Plk1 (+/lox) NSCs in the presence of vehicle (-) or Tam, and Plk1 (+/K i ) NSCs in the presence of vehicle (-) or Dox, represented in arbitrary units (a.u.) after normalisation to the loading control (N = 6, Plk1 (+/lox) ; N = 3, Plk1 (+/K i ) in both treatment conditions, respectively). ( E ) Levels of Cyclin D2 normalised to the loading control in extracts from Plk1 (+/lox) NSCs in the presence of vehicle (-) or Tam (N = 3, in both treatment conditions), and Plk1 (+/K i ) NSCs in the presence of vehicle (-) or Dox (N = 5, in both treatment conditions), represented in arbitrary units (a.u.). ( F ) Representative immunoblots of the protein levels of PLK1-cerulean, Ascl1-myc and VINCULIN (loading control) in lysates obtained from HEK293T cells co-transfected with myc -tagged Ascl1 and either wild type human version of PLK1-cerulean (PLK1 WT -cer), its kinase-dead mutant (PLK1 K82R -cer) or a constitutively active mutant (PLK1 T210D -cer). Cells co-transfected with an empty vector (vector) and untransfected cells (-) were used as controls. The asterisk indicates a non-specific band detected by the Plk1 antibody at 110 kDa. ( G ) Densitometric quantification of Ascl1- myc normalised to loading controls and expressed as arbitrary units (a.u.) in HEK293T cells co-transfected with Ascl1- myc and either PLK1 WT -cer or mutants PLK1 K82R -cer or PLK1 T210D -cer. N = 7 independent transfections for each condition. ( H ) Representative confocal images of the immunodetection of Ascl1- myc (gray) in transfected HeLa cells in mitosis (yellow dashed lines) treated with MG-132, the Plk1 inhibitor BI 6727 or HUWE1 inhibitor BI 8626. Note the typical monopolar spindle-morphology provoked by the full inhibition of PLK1. ( I ) Mean fluorescence intensity (MFI) of Ascl1- myc in mitotic HeLa cells (n) treated with the different inhibitors (n = 74, 77, 70 and 67 independent cells, respectively) in N = 4 independent transfection experiments. ( J ) HUWE1 immunoprecipitation in HEK293T cells transfected with the indicated constructs, arrested in mitosis with nocodazole and treated with MG-132. A representative experiment showing interaction of HUWE1 with Plk1 and with Ascl1 is shown, out of three performed with similar results. Irrelevant lanes have been cropped out of the image (dashed black lines). ( K ) Representative immunoblots of PLK1-cerulean, PLK1 and Ascl1- myc protein levels obtained from untreated or MG-132-treated HEK293T cells co-transfected with myc -tagged Ascl1 and either wild type PLK1-cerulean or its mutant versions. Cells co-transfected with an empty vector (vector) and untransfected (-) cells were used as controls. Alpha-TUBULIN levels are shown as loading control and β-CATENIN and higher molecular weight ubiquitylated forms are shown as control for proteasome inhibition. ( L ) Levels of Ascl1- myc normalised to the loading control represented in arbitrary units (a.u.), in extracts from untreated or MG-132-treated HEK293T cells, co-transfected with Ascl1-myc and either the wild type or mutant versions of PLK1 . N = 6 for each condition. ( M ) Confocal micrographs of the staining for Ascl1 (gray) in control or BI 6727-treated wild-type mice. Cell nuclei were labelled with DAPI (blue). The white dashed lines delimit the SEZ. LV, lateral ventricle. Single channel images and insets (delimited by yellow dashed lines) for the staining of Ascl1 (right panels, gray, yellow arrowheads point at positive cells). Scale bars: 20 µm; inset: 10 µm. ( N ) Quantification of the percentage of Ascl1 + cells in the SEZ of control (N = 4) or BI 6727-treated (N = 4) wild-type mice. ( O ) Normalized mean fluorescence intensity (MFI) of Ascl1 per cell (n) in the SEZ of vehicle- (control; n = 318) or BI 6727-treated (n = 306) mice (N; N = 4 each). *P< 0.05, **p< 0.01 and ***p < 0.001, one-way ANOVA with Dunnett’s multiple comparison test ( B, G, I ), two-tailed unpaired Student’s t -tests ( D, E, N ), two-way ANOVA followed by Šidák’s multiple comparisons test ( L ) and Mann-Whitney’s test ( O ). Data are represented as box and whiskers from min. to max and all data points are shown ( B , D, E, G, L N and O ). Symbols represent mean values from independent neurosphere cultures obtained from individual mice ( B , D, E ), independent transfection experiments ( G, L ), independent mice ( N ) or individual cells ( O ). In ( I ) small symbols represent individual cells ( n ), and bigger symbols represent the mean values of each independent transfection experiment ( N ) and combined in a superplot representation. For full Western blot images refer to .

Article Snippet: To conditionally inactivate Plk1 in NSCs, male Plk1 (lox/lox) mice were crossed with females expressing Cre recombinase downstream of the murine glial fibrillary acidic protein ( Gfap ) promoter, obtained from Jackson Laboratories (Tg(Gfap-cre)73.12Mvs/J) ( Garcia et al ., 2004 ), to generate Plk1 (+/lox) ;Gfap (+/Cre) mice, and are referred herein to as Plk1 Gfap(+/ Δ) .

Techniques: Western Blot, Control, Transfection, Mutagenesis, Plasmid Preparation, Immunodetection, Inhibition, Fluorescence, Immunoprecipitation, Construct, Molecular Weight, Staining, Comparison, Two Tailed Test

Journal: bioRxiv

Article Title: Polo-like kinase 1 controls activation of adult neural stem cells and represents a druggable entry-point to boost adult neurogenesis

doi: 10.64898/2026.05.12.724486

Figure Lengend Snippet: Immunoprecipitation (IP) of PLK1 and Myc, showing the reciprocal interaction between Ascl1 and PLK1, and their interaction with HUWE1 in mitosis HEW293T cells. Representative immunoblots (IB) for the specific detection of HUWE1, PLK1 and Ascl1- myc in samples immunoprecipitated for PLK1 and Myc in lysates from transfected cells. IgG, isotype control antibody. One representative experiment out of three performed with similar results is shown.

Article Snippet: To conditionally inactivate Plk1 in NSCs, male Plk1 (lox/lox) mice were crossed with females expressing Cre recombinase downstream of the murine glial fibrillary acidic protein ( Gfap ) promoter, obtained from Jackson Laboratories (Tg(Gfap-cre)73.12Mvs/J) ( Garcia et al ., 2004 ), to generate Plk1 (+/lox) ;Gfap (+/Cre) mice, and are referred herein to as Plk1 Gfap(+/ Δ) .

Techniques: Immunoprecipitation, Western Blot, Transfection, Control

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: Molecular dynamics results of NC and PLK1. (A) Three-dimensional representation of the protein–ligand complex. The overall protein structure is shown in cartoon format (left), with the ligand depicted as sticks within the binding pocket. The right panel shows an enlarged view of the binding site, highlighting the spatial arrangement of the ligand and surrounding amino acid residues (e.g., LEU-59, LEU-132, LYS-82, PHE-183, and ASP-194), along with the distances of their interactions. (B) Summary of protein–ligand interaction analysis. The table presents hydrophobic interactions, hydrogen bonds, and π-stacking interactions, including details such as interacting residues, atom indices, interaction distances, angles, and related geometric parameters.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: Binding Assay

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: Molecular dynamics results of NC and PLK1. (A) Root mean square deviation (RMSD) of the complex, protein, and ligand as a function of simulation time. (B) Root mean square fluctuation (RMSF) of protein residues. (C) Solvent-accessible surface area (SASA) of the complex over time. (D) Radius of gyration (Rg) of the complex during the simulation. (E) Number of hydrogen bonds formed between the protein and ligand over time. (F) Gibbs free energy landscape as a function of RMSD and Rg, presented in both 2D contour and 3D surface plots. (G) Binding free energy components, including van der Waals, electrostatic, polar solvation, nonpolar solvation, and total energy contributions. (H) Per-residue binding energy contribution of amino acids to the ligand. (I) Representative structures of the protein–ligand complex at 0 ns, 50 ns, and 100 ns during the simulation. NC, Nitidine Chloride; PLK1, polo-like kinase 1; PCA, principal component analysis; RMSD, root mean square deviation; Rg, radius of gyration; RMSF, root mean square fluctuation.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: Solvent, Binding Assay, Residue

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: Single-cell identification of malignant cell populations and proliferation-associated gene expression in colorectal cancer (CRC). (A) UMAP visualization showing the major cell populations in CRC samples, including B cells, cancer-associated fibroblasts (CAFs), endothelial cells, macrophages, malignant epithelial cells, and T/NK cells. (B) Identification of malignant cells based on inferred copy number variation (CNV). The left panel shows the distribution of high-CNV (malignant) and low-CNV (normal-like) cells in UMAP space, while the right panel presents total CNV scores across different cell types or malignant epithelial subpopulations. (C) UMAP feature plots showing the expression patterns of the proliferation-related genes MKI67 and PLK1 at the single-cell level in CRC samples.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: Single Cell, Gene Expression, Expressing

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: Batch effect assessment and correction in the integrated multi-platform colon cancer gene expression dataset for PLK1 biomarker analysis.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: Gene Expression, Biomarker Discovery

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: PLK1 is highly expressed at the mRNA level in CRC (non-CRC: 1260 samples; CRC: 2259 samples). (A) Inclusion flowchart of mRNA datasets. (B) SMD diagram, funnel plot, and SROC diagram. PLK1: polo-like kinase 1; CRC, colorectal cancer; SMD, standardized mean difference; SROC, summary receiver operating characteristic.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques:

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: GSEA analysis of PLK1-coexpressed genes in CRC (R>0.5, P<0.05). (A) Pathway enrichment results. (B) Enrichment pathway network diagram. It shows the relationship between various pathways; the node size represents the number of gene sets, and the color represents the enrichment intensity, revealing that PLK1 is mainly involved in the cell cycle regulatory network. PLK1: polo-like kinase 1; CRC, colorectal cancer; GSEA, Gene Set Enrichment Analysis.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques:

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: PLK1 is highly expressed at the protein level in CRC. (A) Immunohistochemical staining. (B) Expression density distribution diagram. (C) Comparison of expression levels. (D) ROC curve analysis. Data in B-D are from Proteomic Data Commons (30 normal cases vs 42 CRC cases). PLK1, polo-like kinase 1; CRC, colorectal cancer; ROC, receiver operating characteristic.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: Immunohistochemical staining, Staining, Expressing, Comparison

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: Spatial transcriptomics reveals PLK1-related spatial distribution patterns and microenvironmental features in tumor tissue. (A) Spatial maps showing LogTPM expression of proliferation markers PLK1 and MKI67, neutrophil fraction, and inferred cell-type fractions (malignant, macrophage, endothelial, CAF, plasma, B cell, CD4 + T cell, CD8 + T cell, NK cell, cDC, pDC, and mast cell). (B) Correlation heatmap of cell-type abundances estimated by multiple deconvolution algorithms (CIBERSORT, CIBERSORT_ABS, EPIC, ESTIMATE, MCPcounter, Quantiseq, TIMER, xCell) across GEO datasets. (C) Histogram of permuted Lee’s L spatial statistic (observed L = −0.156).

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: Spatial Transcriptomics, Expressing, Clinical Proteomics

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: Knockdown of PLK1 inhibits CRC-related cells. A negative CRISPR score indicates that the gene is essential for cell survival, and a more negative score indicates a more significant inhibition of cell growth after knockdown. PLK1, polo-like kinase 1; CRC, colorectal cancer; CRISPR, clustered regularly interspaced short palindromic repeats.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: Knockdown, CRISPR, Inhibition

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: PLK1 is downregulated at the mRNA and protein levels after NC treatment. (A) Transcriptome sequencing verification. The mRNA expression of PLK1 in HCT116 cells was significantly downregulated after NC treatment. P < 0.01 vs control group. (B) RT-qPCR verification. The mRNA expression level of PLK1 was significantly reduced after treatment with NC (6 μmol/L) for 48h. Data are expressed as mean ± standard deviation. ***P < 0.001 vs control group. (C) In vivo immunohistochemical verification. Detection of PLK1 protein expression in ectopic xenograft tissues of mice. NC downregulated PLK1 protein expression in a dose-dependent manner, and the bar chart in the lower right corner shows the quantitative analysis of the average optical density value of each group. ***P < 0.001 vs control group. NC, Nitidine Chloride; PLK1, polo-like kinase 1.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: Sequencing, Expressing, Control, Quantitative RT-PCR, Standard Deviation, In Vivo, Immunohistochemical staining

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: MYCN directly binds to the PLK1 promoter and both genes are downregulated by Nitidine Chloride. (A) Genome browser tracks showing MYCN ChIP-seq signal and H3K27ac enrichment across the PLK1 genomic locus. The genomic coordinates and gene annotation are shown below. (B) Sequence logo representing the predicted MYCN–MAX binding motif (E-box) identified within the PLK1 promoter region. (C) Structural model of the MYCN–MAX complex in association with the PLK1 promoter DNA sequence generated by AlphaFold-Multimer and protein–DNA docking. The structure is colored according to pLDDT confidence scores. (D) Predicted aligned error (PAE) plot of the MYCN–MAX complex, indicating the confidence of relative positioning between residues.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: ChIP-sequencing, Sequencing, Binding Assay, Generated

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: High MYCN mRNA expression in CRC. (A) Forest plot showing the standardized mean difference (SMD) in MYCN mRNA expression levels between CRC (experimental) and normal control groups across multiple studies/datasets, with pooled estimates for common-effect and random-effects models, heterogeneity statistics, summary receiver operating characteristic (SROC) curve, and publication bias tests (Egger’s and Begg’s). (B) Heatmap of Pearson correlation coefficients (R) between PLK1 and MYCN mRNA expression across the listed studies (significant correlations marked with asterisks).

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: Expressing, Control