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ATCC pc9 egfr
Pc9 Egfr, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 4444 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 99 stars, based on 4444 article reviews

pc9 egfr - by Bioz Stars, 2026-05

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Experimental validation of the function of ACTN1 in inducing EGFR-TKI resistance and malignant phenotypes in the PC9 cell line. (A) Osimertinib-resistant and parental PC9 lung adenocarcinoma cell lines (designated PC9-P and PC9-OR) are treated with osimertinib, followed by CCK-8 assays. (B) Representative images of PC9-P and PC9-OR cells under a 10× microscope. (C) A bar plot reveals the result of qPCR, illustrating relative mRNA expression levels of ACTN1 in PC9-P and PC9-OR cell lines. (D,E) Western blotting shows ACTN1-silencing efficiency in PC9-OR cells. Quantification is performed using ImageJ software. (F) PC9-OR and ACTN1-silenced PC9-OR cells are treated with osimertinib, and their sensitivities are assessed by CCK-8 assays. (G) CCK8-assays are conducted in primary and ACTN1-silenced PC9-OR cells. Cellular viabilities of all cell groups within 5 days are quantified by optical density (OD) values at 450 nm and depicted in a line chart. (H,I) Transwell migration assays are conducted in primary and ACTN1-silenced PC9-OR cells. The number of migration cells are counted using ImageJ software. ( p -value ≥0.05, ns; p -value <0.05, *; p -value <0.01, **; p -value <0.001, ***; p -value <0.0001, ****).

Journal: Frontiers in Cell and Developmental Biology

Article Title: Integrative single-cell and bulk RNA sequencing unravels the role of ACTN1 in promoting lung cancer with brain metastasis and epidermal growth factor receptor-tyrosine kinase inhibitor resistance

doi: 10.3389/fcell.2026.1738641

Figure Lengend Snippet: Experimental validation of the function of ACTN1 in inducing EGFR-TKI resistance and malignant phenotypes in the PC9 cell line. (A) Osimertinib-resistant and parental PC9 lung adenocarcinoma cell lines (designated PC9-P and PC9-OR) are treated with osimertinib, followed by CCK-8 assays. (B) Representative images of PC9-P and PC9-OR cells under a 10× microscope. (C) A bar plot reveals the result of qPCR, illustrating relative mRNA expression levels of ACTN1 in PC9-P and PC9-OR cell lines. (D,E) Western blotting shows ACTN1-silencing efficiency in PC9-OR cells. Quantification is performed using ImageJ software. (F) PC9-OR and ACTN1-silenced PC9-OR cells are treated with osimertinib, and their sensitivities are assessed by CCK-8 assays. (G) CCK8-assays are conducted in primary and ACTN1-silenced PC9-OR cells. Cellular viabilities of all cell groups within 5 days are quantified by optical density (OD) values at 450 nm and depicted in a line chart. (H,I) Transwell migration assays are conducted in primary and ACTN1-silenced PC9-OR cells. The number of migration cells are counted using ImageJ software. ( p -value ≥0.05, ns; p -value <0.05, *; p -value <0.01, **; p -value <0.001, ***; p -value <0.0001, ****).

Article Snippet: Briefly, parental PC9 cells in the logarithmic growth phase were exposed to gradually increasing concentration of osimertinib (#HY-15772, MedChemExpress, China).

Techniques: Biomarker Discovery, CCK-8 Assay, Microscopy, Expressing, Western Blot, Software, Migration

a, Design of a gRNA (EGFRdel g) targeting the EGFR E746_A750del mutant transcript. b, Testing of the EGFRdel-specific gRNA in PC9 NSCLC cells (EGFR E746_A750del) and RPE1 cells (EGFR WT) stably expressing Cas12a2. c , Growth curves of PC9 and RPE1 cells after targeting EGFR E746_A750del mutant transcript. d , Fold-increase in cell number over 96 h following Cas12a2 targeting of the EGFR E746_A750del mutant transcript in PC9 and RPE1 cells. e, Immunoblots showing expression of DNA damage markers in PC9 and RPE1 cells 48 h following Cas12a2 targeting of the EGFR E746_A750del mutant transcript. Statistics: ****p<0.0001; ns, non-significant, one-way ANOVA with Dunnett’s test.

Journal: bioRxiv

Article Title: Selective Elimination of TP53 Mutant Cells by Transcript-Activated Chromatin Shredding

doi: 10.64898/2026.05.08.723607

Figure Lengend Snippet: a, Design of a gRNA (EGFRdel g) targeting the EGFR E746_A750del mutant transcript. b, Testing of the EGFRdel-specific gRNA in PC9 NSCLC cells (EGFR E746_A750del) and RPE1 cells (EGFR WT) stably expressing Cas12a2. c , Growth curves of PC9 and RPE1 cells after targeting EGFR E746_A750del mutant transcript. d , Fold-increase in cell number over 96 h following Cas12a2 targeting of the EGFR E746_A750del mutant transcript in PC9 and RPE1 cells. e, Immunoblots showing expression of DNA damage markers in PC9 and RPE1 cells 48 h following Cas12a2 targeting of the EGFR E746_A750del mutant transcript. Statistics: ****p<0.0001; ns, non-significant, one-way ANOVA with Dunnett’s test.

Article Snippet: PC9 cells were injected intravenously into the tail vein of NOD.Cg- Prkdc scid Il2rg tm1Wjl /SzJ (NSG) mice (Jackson Laboratory, Strain no. 005557) in 0.1-0.2 mL PBS to generate orthotopic tumors of NSCLC.

Techniques: Mutagenesis, Stable Transfection, Expressing, Western Blot

a, Mutational spectrum of the p53 protein in tumor samples from 3,949 cancer patients from TCGA Pan-Cancer Atlas studies in the cBioPortal database. M246, R248, R280 and E285 residues targeted in this study are highlighted. b, Design of a gRNA (R248Q g) targeting the p53 R248Q mutant transcript. PFS, protospacer flanking site. c, Fold-increase in cell number over 96 h following Cas12a2 targeting of the p53 R248Q mutant transcript in RPE1 cells expressing p53 R248Q (RPE1 p53 R248Q), wild-type RPE1 cells (RPE1 WT) and d, PC9 cells. Cas12a2 was stably expressed in these cells. e , Growth competition assay between RPE1 WT and R248Q cells. f, Immunoblots showing expression of DNA damage markers in cells 48 h following Cas12a2 targeting of the p53 R248Q mutant transcript. Statistics: *p<0.05; **p<0.01; ****p<0.0001; ns, non-significant, one-way ANOVA with Dunnett’s test.

Journal: bioRxiv

Article Title: Selective Elimination of TP53 Mutant Cells by Transcript-Activated Chromatin Shredding

doi: 10.64898/2026.05.08.723607

Figure Lengend Snippet: a, Mutational spectrum of the p53 protein in tumor samples from 3,949 cancer patients from TCGA Pan-Cancer Atlas studies in the cBioPortal database. M246, R248, R280 and E285 residues targeted in this study are highlighted. b, Design of a gRNA (R248Q g) targeting the p53 R248Q mutant transcript. PFS, protospacer flanking site. c, Fold-increase in cell number over 96 h following Cas12a2 targeting of the p53 R248Q mutant transcript in RPE1 cells expressing p53 R248Q (RPE1 p53 R248Q), wild-type RPE1 cells (RPE1 WT) and d, PC9 cells. Cas12a2 was stably expressed in these cells. e , Growth competition assay between RPE1 WT and R248Q cells. f, Immunoblots showing expression of DNA damage markers in cells 48 h following Cas12a2 targeting of the p53 R248Q mutant transcript. Statistics: *p<0.05; **p<0.01; ****p<0.0001; ns, non-significant, one-way ANOVA with Dunnett’s test.

Techniques: Mutagenesis, Expressing, Stable Transfection, Competitive Binding Assay, Western Blot

a, Time-course analysis of in vitro trans -cleavage of FAM-labelled dsDNA by Cas12a2 with R248Q g in the presence of p53 R248Q RNA fragment or p53 WT RNA fragment. b, Schematic of the FUCCI cell cycle reporter. c, Time-lapse images of RPE1 p53 R248Q cells expressing the FUCCI reporter following Cas12a2 targeting of the p53 R248Q mutant transcript. Merged green, red and phase contrast channels are shown. White arrows indicate cells with fragmented nuclei. d, FACS gating of dead cell populations in PC9 LentiCas12a2 cells 96 h following Cas12a2 targeting. e, Quantification of dead cell populations in PC9 LentiCas12a2 cells 96 h following Cas12a2 targeting. Statistics: **p<0.01, one-way ANOVA with Dunnett’s test.

Journal: bioRxiv

Article Title: Selective Elimination of TP53 Mutant Cells by Transcript-Activated Chromatin Shredding

doi: 10.64898/2026.05.08.723607

Figure Lengend Snippet: a, Time-course analysis of in vitro trans -cleavage of FAM-labelled dsDNA by Cas12a2 with R248Q g in the presence of p53 R248Q RNA fragment or p53 WT RNA fragment. b, Schematic of the FUCCI cell cycle reporter. c, Time-lapse images of RPE1 p53 R248Q cells expressing the FUCCI reporter following Cas12a2 targeting of the p53 R248Q mutant transcript. Merged green, red and phase contrast channels are shown. White arrows indicate cells with fragmented nuclei. d, FACS gating of dead cell populations in PC9 LentiCas12a2 cells 96 h following Cas12a2 targeting. e, Quantification of dead cell populations in PC9 LentiCas12a2 cells 96 h following Cas12a2 targeting. Statistics: **p<0.01, one-way ANOVA with Dunnett’s test.

Techniques: In Vitro, Expressing, Mutagenesis

a, Design of a gRNA (R280K g) targeting the p53 R280K mutant transcript. b, Design of a gRNA (E285K g) targeting the p53 E285K mutant transcript. c, Fold-increase in cell number over 96 h following Cas12a2 targeting of p53 R280K or E285K mutant transcripts. d, Immunoblots showing expression of DNA damage marker phospho-KAP1 in RPE1 p53 R280K, RPE1 p53 E285K and RPE1 WT cells 48 h following Cas12a2 targeting of the mutant transcripts. e, Design of gRNAs (M246I g1-6) targeting the p53 M246I mutant transcript. f, Trans -cleavage of purified genomic DNA by Cas12a2 with M246I gRNAs in the presence of the mutant target RNA or WT target RNA. g , Fold-increase in green intensity over 96 h following Cas12a2 targeting of the p53 M246I mutant transcript in NCI-H23 cells (p53 M246I) and U2OS cells (p53 WT) expressing Cas12a2-2A-EGFP. h, Analysis of mutation types in the TP53 coding sequence (CDS) from 16,708 tumor samples. Although Cas12a2 prefers an A-rich PFS , a consensus PFS sequence could not be built . However, we noticed that a single adenine nucleotide can sometimes serve as a PFS to activate Cas12a2 , and more adenine bases between the -2 to -4 position at the 3’ end of the protospacer can lead to higher Cas12a2 activity ( and ). 25.7% of TP53 mutations in patients are B-to-A substitutions (where B is G, C, or T) , which could serve as new or enhanced PFS for targeting, as demonstrated with the R248Q mutation . 17.1% of TP53 mutations are base insertions or deletions , offering opportunities for targeting similar to our approach with the EGFR in-frame deletion mutation . i, Frequency of the presence of A, AA or ANA within 24 nt at the 3’ end of TP53 mutations from 16, 708 tumor samples. Tumor sample data in c and d are from TCGA Pan-Cancer Atlas studies and MSK-CHORD studies. j, Cas12a2 targeting by transfecting mRNA encoding Cas12a2 and gRNAs into PC9 cells. Growth curves and fold-increase in cell number over 96 h are shown on the right. h, Characterization of LNPs used for the in vivo lung tumor treatment test. Statistics: **p<0.01; ****p<0.0001; ns, non-significant, one-way ANOVA with Dunnett’s test.

Journal: bioRxiv

Article Title: Selective Elimination of TP53 Mutant Cells by Transcript-Activated Chromatin Shredding

doi: 10.64898/2026.05.08.723607

Figure Lengend Snippet: a, Design of a gRNA (R280K g) targeting the p53 R280K mutant transcript. b, Design of a gRNA (E285K g) targeting the p53 E285K mutant transcript. c, Fold-increase in cell number over 96 h following Cas12a2 targeting of p53 R280K or E285K mutant transcripts. d, Immunoblots showing expression of DNA damage marker phospho-KAP1 in RPE1 p53 R280K, RPE1 p53 E285K and RPE1 WT cells 48 h following Cas12a2 targeting of the mutant transcripts. e, Design of gRNAs (M246I g1-6) targeting the p53 M246I mutant transcript. f, Trans -cleavage of purified genomic DNA by Cas12a2 with M246I gRNAs in the presence of the mutant target RNA or WT target RNA. g , Fold-increase in green intensity over 96 h following Cas12a2 targeting of the p53 M246I mutant transcript in NCI-H23 cells (p53 M246I) and U2OS cells (p53 WT) expressing Cas12a2-2A-EGFP. h, Analysis of mutation types in the TP53 coding sequence (CDS) from 16,708 tumor samples. Although Cas12a2 prefers an A-rich PFS , a consensus PFS sequence could not be built . However, we noticed that a single adenine nucleotide can sometimes serve as a PFS to activate Cas12a2 , and more adenine bases between the -2 to -4 position at the 3’ end of the protospacer can lead to higher Cas12a2 activity ( and ). 25.7% of TP53 mutations in patients are B-to-A substitutions (where B is G, C, or T) , which could serve as new or enhanced PFS for targeting, as demonstrated with the R248Q mutation . 17.1% of TP53 mutations are base insertions or deletions , offering opportunities for targeting similar to our approach with the EGFR in-frame deletion mutation . i, Frequency of the presence of A, AA or ANA within 24 nt at the 3’ end of TP53 mutations from 16, 708 tumor samples. Tumor sample data in c and d are from TCGA Pan-Cancer Atlas studies and MSK-CHORD studies. j, Cas12a2 targeting by transfecting mRNA encoding Cas12a2 and gRNAs into PC9 cells. Growth curves and fold-increase in cell number over 96 h are shown on the right. h, Characterization of LNPs used for the in vivo lung tumor treatment test. Statistics: **p<0.01; ****p<0.0001; ns, non-significant, one-way ANOVA with Dunnett’s test.

Techniques: Mutagenesis, Western Blot, Expressing, Marker, Purification, Sequencing, Activity Assay, In Vivo

a-b, Cas12a2 targeting of p53 R248Q transcripts by delivering LNP packaging mRNA encoding Cas12a2 and gRNAs into PC9 cells. Fold-increase in cell number over 96 h is shown on the right. c, Schematic showing in vivo treatment of MYC-induced liver tumors. Plasmids expressing the MYC oncogene and Sleeping Beauty transposases were introduced into mice by hydrodynamic tail vein injection (HDTVi), resulting in stable integration of MYC into random liver cells. d, Quantification of liver tumor surface area as the percentage of whole liver surface area. e, Schematic showing in vivo treatment of PC9 lung tumors. The inoculated PC9 cells express firefly luciferase (Fluc) for live animal imaging. f , Quantification of tumor bioluminescence signals over time in treated mice. g, Schematic showing Cas12a2-mediated selective cell elimination. Statistics: *p<0.05; ns, non-significant, Student’s t-test.

Journal: bioRxiv

Article Title: Selective Elimination of TP53 Mutant Cells by Transcript-Activated Chromatin Shredding

doi: 10.64898/2026.05.08.723607

Figure Lengend Snippet: a-b, Cas12a2 targeting of p53 R248Q transcripts by delivering LNP packaging mRNA encoding Cas12a2 and gRNAs into PC9 cells. Fold-increase in cell number over 96 h is shown on the right. c, Schematic showing in vivo treatment of MYC-induced liver tumors. Plasmids expressing the MYC oncogene and Sleeping Beauty transposases were introduced into mice by hydrodynamic tail vein injection (HDTVi), resulting in stable integration of MYC into random liver cells. d, Quantification of liver tumor surface area as the percentage of whole liver surface area. e, Schematic showing in vivo treatment of PC9 lung tumors. The inoculated PC9 cells express firefly luciferase (Fluc) for live animal imaging. f , Quantification of tumor bioluminescence signals over time in treated mice. g, Schematic showing Cas12a2-mediated selective cell elimination. Statistics: *p<0.05; ns, non-significant, Student’s t-test.

Techniques: In Vivo, Expressing, Injection, Luciferase, Imaging

a, Schematic showing the Ai9 Cre-dependent tdTomato reporter system. The reporter construct was integrated into PC9 cells by the Sleeping Beauty transposase. Cells were selected by puromycin. b, Flow cytometry analysis showing tdTomato expression in PC9 Ai9 cells after treating them with LNPs delivering Cre mRNA in vitro . c, Fluorescent histological images of a mouse lung 53 days post engraftment with PC9 zsGreen-Fluc cells. d, IVIS image of a mouse injected with PC9 zsGreen-Fluc cells. e, Schematic illustrating delivery efficiency assessment of LNPs to PC9 lung tumors. Each mouse received 20 μg Cre mRNA delivered by LNP. f and g, Flow cytometry analysis of isolated PC9 zsGreen Ai9 cells from mouse lung tissues after LNP Cre mRNA delivery as shown in e. Quantification of the percentage of tdTomato+ cells is shown in g (n=3 mice).

Journal: bioRxiv

Article Title: Selective Elimination of TP53 Mutant Cells by Transcript-Activated Chromatin Shredding

doi: 10.64898/2026.05.08.723607

Figure Lengend Snippet: a, Schematic showing the Ai9 Cre-dependent tdTomato reporter system. The reporter construct was integrated into PC9 cells by the Sleeping Beauty transposase. Cells were selected by puromycin. b, Flow cytometry analysis showing tdTomato expression in PC9 Ai9 cells after treating them with LNPs delivering Cre mRNA in vitro . c, Fluorescent histological images of a mouse lung 53 days post engraftment with PC9 zsGreen-Fluc cells. d, IVIS image of a mouse injected with PC9 zsGreen-Fluc cells. e, Schematic illustrating delivery efficiency assessment of LNPs to PC9 lung tumors. Each mouse received 20 μg Cre mRNA delivered by LNP. f and g, Flow cytometry analysis of isolated PC9 zsGreen Ai9 cells from mouse lung tissues after LNP Cre mRNA delivery as shown in e. Quantification of the percentage of tdTomato+ cells is shown in g (n=3 mice).

Techniques: Construct, Flow Cytometry, Expressing, In Vitro, Injection, Isolation

a, Schematic showing late-stage lung tumor treatment scheme. b, Representative IVIS images of mice bearing Fluc-expressing PC9 cells. Bioluminescence signals outside the lung are considered from metastasis. c, Quantification of tumor bioluminescence signals in the lung and outside the lung over time in treated mice in a .

Journal: bioRxiv

Article Title: Selective Elimination of TP53 Mutant Cells by Transcript-Activated Chromatin Shredding

doi: 10.64898/2026.05.08.723607

Figure Lengend Snippet: a, Schematic showing late-stage lung tumor treatment scheme. b, Representative IVIS images of mice bearing Fluc-expressing PC9 cells. Bioluminescence signals outside the lung are considered from metastasis. c, Quantification of tumor bioluminescence signals in the lung and outside the lung over time in treated mice in a .

Techniques: Expressing

USP5 promotes malignant proliferation and tumor growth in LUAD (A) Western blot analysis of USP5 protein levels in H1299, PC9, and H1650 cells following lentiviral-mediated knockdown or overexpression. (B) Representative images and quantification of EdU incorporation assays evaluating proliferative activity upon USP5 modulation. (C) Cell viability measured by CCK-8 assays in LUAD cells with USP5 knockdown or overexpression over time. (D) Colony formation capacity of LUAD cells after USP5 modulation (representative images and quantified results). (E) Representative excised tumors from nude mice at the experimental endpoint (day 24 post-injection). (F) Tumor volume measured every 4 days from day 7 post-injection. (G) Final tumor weights and volumes from the xenograft mouse model. Data are expressed as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; triplicate experiments.

Journal: iScience

Article Title: USP5-mediated CD73 deubiquitination drives osimertinib resistance via PI3K/AKT and glycolysis activation in LUAD

doi: 10.1016/j.isci.2026.114916

Figure Lengend Snippet: USP5 promotes malignant proliferation and tumor growth in LUAD (A) Western blot analysis of USP5 protein levels in H1299, PC9, and H1650 cells following lentiviral-mediated knockdown or overexpression. (B) Representative images and quantification of EdU incorporation assays evaluating proliferative activity upon USP5 modulation. (C) Cell viability measured by CCK-8 assays in LUAD cells with USP5 knockdown or overexpression over time. (D) Colony formation capacity of LUAD cells after USP5 modulation (representative images and quantified results). (E) Representative excised tumors from nude mice at the experimental endpoint (day 24 post-injection). (F) Tumor volume measured every 4 days from day 7 post-injection. (G) Final tumor weights and volumes from the xenograft mouse model. Data are expressed as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; triplicate experiments.

Article Snippet: PC9 cell line , ServiceBio Co., Ltd. (Hubei, China) , Cat#STCC10210P.

Techniques: Western Blot, Knockdown, Over Expression, Activity Assay, CCK-8 Assay, Injection

USP5 drives aggressive malignant phenotypes in LUAD by enhancing invasion, suppressing apoptosis, and inducing EMT (A) Wound healing assays demonstrating that USP5 knockdown impairs migration in H1299 cells, while its overexpression enhances migration in H1650 cells. Scale bars: 100 μm. (B) Transwell invasion assays showing that USP5 knockdown reduces invasion, whereas its overexpression increases invasion in the respective cell lines. Scale bars: 100 μm. (C) Flow cytometric analysis indicating that USP5 knockdown promotes apoptosis in H1299 and PC9 cells. (D) Western blot analysis of epithelial-mesenchymal transition and apoptosis-related protein expression following USP5 knockdown in H1299 cells. Data are presented as the mean ± SD from n = 3 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 versus the respective control group.

Journal: iScience

Article Title: USP5-mediated CD73 deubiquitination drives osimertinib resistance via PI3K/AKT and glycolysis activation in LUAD

doi: 10.1016/j.isci.2026.114916

Figure Lengend Snippet: USP5 drives aggressive malignant phenotypes in LUAD by enhancing invasion, suppressing apoptosis, and inducing EMT (A) Wound healing assays demonstrating that USP5 knockdown impairs migration in H1299 cells, while its overexpression enhances migration in H1650 cells. Scale bars: 100 μm. (B) Transwell invasion assays showing that USP5 knockdown reduces invasion, whereas its overexpression increases invasion in the respective cell lines. Scale bars: 100 μm. (C) Flow cytometric analysis indicating that USP5 knockdown promotes apoptosis in H1299 and PC9 cells. (D) Western blot analysis of epithelial-mesenchymal transition and apoptosis-related protein expression following USP5 knockdown in H1299 cells. Data are presented as the mean ± SD from n = 3 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 versus the respective control group.

Article Snippet: PC9 cell line , ServiceBio Co., Ltd. (Hubei, China) , Cat#STCC10210P.

Techniques: Knockdown, Migration, Over Expression, Western Blot, Expressing, Control

USP5 interacts with and post-transcriptionally stabilizes CD73 in LUAD (A) Co-immunoprecipitation (CoIP) of USP5 from H1299 lysates followed by mass spectrometry (MS) analysis of Coomassie-stained bands identifies CD73 as a potential interacting partner. (B) Specificity control: CoIP shows no interaction between USP5 and the glycolytic enzymes TPI1, PKM, or PGK1. (C and D) Endogenous coIP confirms the USP5-CD73 interaction in H1299 LUAD cells (C) and PC9 LUAD cells (D). (E–G) Exogenous coIP validates the direct interaction in HEK-293T cells (E and F) and LUAD cells (G) co-expressing Flag-USP5 and His-CD73. (H) USP5 and CD73 protein levels are coordinately upregulated in LUAD cell lines compared to normal bronchial epithelial cells (HBE135-E6E7). (I) USP5 knockdown or overexpression does not alter CD73 mRNA levels (RT-qPCR). (J–M) USP5 positively regulates CD73 protein expression, as shown by its levels upon USP5 knockdown or overexpression. (J and K) CD73 levels decreased upon USP5 knockdown. (L and M) CD73 levels increased upon USP5 overexpression. Data are presented as the mean ± SD from n = 3 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Journal: iScience

Article Title: USP5-mediated CD73 deubiquitination drives osimertinib resistance via PI3K/AKT and glycolysis activation in LUAD

doi: 10.1016/j.isci.2026.114916

Figure Lengend Snippet: USP5 interacts with and post-transcriptionally stabilizes CD73 in LUAD (A) Co-immunoprecipitation (CoIP) of USP5 from H1299 lysates followed by mass spectrometry (MS) analysis of Coomassie-stained bands identifies CD73 as a potential interacting partner. (B) Specificity control: CoIP shows no interaction between USP5 and the glycolytic enzymes TPI1, PKM, or PGK1. (C and D) Endogenous coIP confirms the USP5-CD73 interaction in H1299 LUAD cells (C) and PC9 LUAD cells (D). (E–G) Exogenous coIP validates the direct interaction in HEK-293T cells (E and F) and LUAD cells (G) co-expressing Flag-USP5 and His-CD73. (H) USP5 and CD73 protein levels are coordinately upregulated in LUAD cell lines compared to normal bronchial epithelial cells (HBE135-E6E7). (I) USP5 knockdown or overexpression does not alter CD73 mRNA levels (RT-qPCR). (J–M) USP5 positively regulates CD73 protein expression, as shown by its levels upon USP5 knockdown or overexpression. (J and K) CD73 levels decreased upon USP5 knockdown. (L and M) CD73 levels increased upon USP5 overexpression. Data are presented as the mean ± SD from n = 3 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: PC9 cell line , ServiceBio Co., Ltd. (Hubei, China) , Cat#STCC10210P.

Techniques: Immunoprecipitation, Mass Spectrometry, Staining, Control, Expressing, Knockdown, Over Expression, Quantitative RT-PCR

USP5 reprograms glycolytic metabolism in LUAD (A) Principal component analysis of global metabolic profiles shows a clear separation between the control and USP5-knockdown H1299 cells. (B and C) Unsupervised analysis identifies significantly altered metabolites upon USP5 knockdown, displayed in a volcano plot (B) and heatmap (C). (D) Targeted metabolomics reveals an impaired glycolytic flux in USP5-knockdown cells, as indicated by the concurrent depletion of key glycolytic intermediates, including glucose-6-phosphate (G6P), fructose-6-phosphate (F6P), pyruvate, and lactate. (E–I) Functional assessment of glycolysis using a Seahorse XF Analyzer. USP5 knockdown reduces the proton efflux rate (PER), basal glycolysis, and compensatory glycolysis in H1299 cells (E), PC9 cells (F), and HCC827-OR cells (I); USP5 overexpression enhances these parameters in H1650 cells (G) and HCC827 cells (H). (J) Consistent with the functional data, extracellular lactate secretion decreased by USP5 knockdown and increased by USP5 overexpression. Data are presented as the mean ± SD from n = 3 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 versus the respective control group.

Journal: iScience

Article Title: USP5-mediated CD73 deubiquitination drives osimertinib resistance via PI3K/AKT and glycolysis activation in LUAD

doi: 10.1016/j.isci.2026.114916

Figure Lengend Snippet: USP5 reprograms glycolytic metabolism in LUAD (A) Principal component analysis of global metabolic profiles shows a clear separation between the control and USP5-knockdown H1299 cells. (B and C) Unsupervised analysis identifies significantly altered metabolites upon USP5 knockdown, displayed in a volcano plot (B) and heatmap (C). (D) Targeted metabolomics reveals an impaired glycolytic flux in USP5-knockdown cells, as indicated by the concurrent depletion of key glycolytic intermediates, including glucose-6-phosphate (G6P), fructose-6-phosphate (F6P), pyruvate, and lactate. (E–I) Functional assessment of glycolysis using a Seahorse XF Analyzer. USP5 knockdown reduces the proton efflux rate (PER), basal glycolysis, and compensatory glycolysis in H1299 cells (E), PC9 cells (F), and HCC827-OR cells (I); USP5 overexpression enhances these parameters in H1650 cells (G) and HCC827 cells (H). (J) Consistent with the functional data, extracellular lactate secretion decreased by USP5 knockdown and increased by USP5 overexpression. Data are presented as the mean ± SD from n = 3 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 versus the respective control group.

Article Snippet: PC9 cell line , ServiceBio Co., Ltd. (Hubei, China) , Cat#STCC10210P.

Techniques: Control, Knockdown, Functional Assay, Over Expression

The USP5-CD73 axis drives glycolytic flux by modulating key glycolytic effectors (A) USP5 knockdown reduces, while its overexpression increases, the protein levels of CD73, phosphorylated EGFR ( p -EGFR), and key glycolytic enzymes. (B) CD73 knockdown recapitulates the effect of USP5 knockdown on p -EGFR and glycolytic effector expression. (C) Osimertinib-resistant HCC827-RO cells exhibit elevated levels of USP5, CD73, p -EGFR, and glycolytic proteins compared to their sensitive counterparts. (D and E) Functional assessment of glycolysis using a Seahorse XF Analyzer. (D) CD73 knockdown reduces the proton efflux rate (PER), basal glycolysis, and compensatory glycolysis in H1299 cells. (E) CD73 knockdown reduces the PER, basal glycolysis, and compensatory glycolysis in PC9 cells. (F and G) Reconstitution of CD73 expression in USP5-knockdown H1299 cells (F) and USP5-knockdown PC9 cells (G) rescues the impaired glycolytic function. (H and I) Consistent with the functional assays, CD73 knockdown decreases extracellular lactate secretion (H), while CD73 overexpression restores extracellular lactate secretion (I) in USP5-deficient cells. Data are presented as the mean ± SD from n = 3 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 versus the respective control group.

Journal: iScience

Article Title: USP5-mediated CD73 deubiquitination drives osimertinib resistance via PI3K/AKT and glycolysis activation in LUAD

doi: 10.1016/j.isci.2026.114916

Figure Lengend Snippet: The USP5-CD73 axis drives glycolytic flux by modulating key glycolytic effectors (A) USP5 knockdown reduces, while its overexpression increases, the protein levels of CD73, phosphorylated EGFR ( p -EGFR), and key glycolytic enzymes. (B) CD73 knockdown recapitulates the effect of USP5 knockdown on p -EGFR and glycolytic effector expression. (C) Osimertinib-resistant HCC827-RO cells exhibit elevated levels of USP5, CD73, p -EGFR, and glycolytic proteins compared to their sensitive counterparts. (D and E) Functional assessment of glycolysis using a Seahorse XF Analyzer. (D) CD73 knockdown reduces the proton efflux rate (PER), basal glycolysis, and compensatory glycolysis in H1299 cells. (E) CD73 knockdown reduces the PER, basal glycolysis, and compensatory glycolysis in PC9 cells. (F and G) Reconstitution of CD73 expression in USP5-knockdown H1299 cells (F) and USP5-knockdown PC9 cells (G) rescues the impaired glycolytic function. (H and I) Consistent with the functional assays, CD73 knockdown decreases extracellular lactate secretion (H), while CD73 overexpression restores extracellular lactate secretion (I) in USP5-deficient cells. Data are presented as the mean ± SD from n = 3 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 versus the respective control group.

Article Snippet: PC9 cell line , ServiceBio Co., Ltd. (Hubei, China) , Cat#STCC10210P.

Techniques: Knockdown, Over Expression, Expressing, Functional Assay, Control

CD73 is a critical downstream effector for USP5-mediated oncogenic phenotypes in LUAD (A and C) USP5 knockdown in H1299 cells (A) and PC9 cells (C) impairs migration, invasion, and colony formation. These phenotypic defects are rescued by the concomitant overexpression of CD73, as assessed by transwell, wound healing, and colony formation assays (scale bars: 100 μm). (B and D) Cell viability (CCK-8 assays) in H1299 cells (B) and PC9 cells (D) is reduced upon USP5 knockdown but is restored by CD73 overexpression. Data are presented as the mean ± SD from n = 3 independent experiments; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Statistical comparisons are shown for relevant groups.

Journal: iScience

Article Title: USP5-mediated CD73 deubiquitination drives osimertinib resistance via PI3K/AKT and glycolysis activation in LUAD

doi: 10.1016/j.isci.2026.114916

Figure Lengend Snippet: CD73 is a critical downstream effector for USP5-mediated oncogenic phenotypes in LUAD (A and C) USP5 knockdown in H1299 cells (A) and PC9 cells (C) impairs migration, invasion, and colony formation. These phenotypic defects are rescued by the concomitant overexpression of CD73, as assessed by transwell, wound healing, and colony formation assays (scale bars: 100 μm). (B and D) Cell viability (CCK-8 assays) in H1299 cells (B) and PC9 cells (D) is reduced upon USP5 knockdown but is restored by CD73 overexpression. Data are presented as the mean ± SD from n = 3 independent experiments; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Statistical comparisons are shown for relevant groups.

Article Snippet: PC9 cell line , ServiceBio Co., Ltd. (Hubei, China) , Cat#STCC10210P.

Techniques: Knockdown, Migration, Over Expression, CCK-8 Assay

NTRK2 promotes malignant behavior of LUAD cells in vitro . (A) The expression of NTRK2 was verified by qRT-PCR at the transcriptional level in A549, A549/Taxol and PC9 cells. (B) Western blotting analysis was performed to validate the expression of NTRK2 protein in the above cells. (C) MTT showing the effect of NTRK2 knockdown on the proliferation of A549, A549/Taxol and PC9 cells. Data are shown as mean ± SD. Statistical analysis was performed by two-way ANOVA. (D) The effect of NTRK2 knockdown on colony formation ability of the above cells. The right histograms showed the number of colonies for each cell line as indicated. (E) Relative mRNA expression level of NTRK2 was determined by qRT-PCR in A549 and PC9 cells transfected with an empty vector (Vector) or an NTRK2-overexpressing plasmid (oe-NTRK2). (F) Protein expression level of NTRK2 was analyzed by Western blotting in the same set of transfected cells. (G) Cell proliferation was assessed by MTT assay in A549 and PC9 cells following NTRK2 overexpression. Data are presented as the mean ± SD. Statistical analysis was performed by two-way ANOVA. (H) The promoting effect of NTRK2 overexpression on colony formation in A549 and PC9 cells. The effect of NTRK2 knockdown on cell cycle distributions (I) and apoptosis (J) was examined by the flow cytometry. The histograms of cell cycle distributions and apoptosis are presented on the right side of their respective representative graphs. Data are presented as the mean ± SD. β-actin was used as an internal control for qRT-PCR. GAPDH was adopted as the internal control for Western blotting. * P < 0.05; ** P < 0.01; *** P < 0.001.

Journal: Translational Oncology

Article Title: NTRK2 promotes malignant progression and paclitaxel resistance of lung adenocarcinoma through targeting MYC/ABCF1 axis

doi: 10.1016/j.tranon.2025.102655

Figure Lengend Snippet: NTRK2 promotes malignant behavior of LUAD cells in vitro . (A) The expression of NTRK2 was verified by qRT-PCR at the transcriptional level in A549, A549/Taxol and PC9 cells. (B) Western blotting analysis was performed to validate the expression of NTRK2 protein in the above cells. (C) MTT showing the effect of NTRK2 knockdown on the proliferation of A549, A549/Taxol and PC9 cells. Data are shown as mean ± SD. Statistical analysis was performed by two-way ANOVA. (D) The effect of NTRK2 knockdown on colony formation ability of the above cells. The right histograms showed the number of colonies for each cell line as indicated. (E) Relative mRNA expression level of NTRK2 was determined by qRT-PCR in A549 and PC9 cells transfected with an empty vector (Vector) or an NTRK2-overexpressing plasmid (oe-NTRK2). (F) Protein expression level of NTRK2 was analyzed by Western blotting in the same set of transfected cells. (G) Cell proliferation was assessed by MTT assay in A549 and PC9 cells following NTRK2 overexpression. Data are presented as the mean ± SD. Statistical analysis was performed by two-way ANOVA. (H) The promoting effect of NTRK2 overexpression on colony formation in A549 and PC9 cells. The effect of NTRK2 knockdown on cell cycle distributions (I) and apoptosis (J) was examined by the flow cytometry. The histograms of cell cycle distributions and apoptosis are presented on the right side of their respective representative graphs. Data are presented as the mean ± SD. β-actin was used as an internal control for qRT-PCR. GAPDH was adopted as the internal control for Western blotting. * P < 0.05; ** P < 0.01; *** P < 0.001.

Article Snippet: Human LUAD cell lines PC9, A549 and its taxol-resistant strain A549/Taxol were purchased from Procell Life Science & Technology Co.,Ltd (Wuhan, China).

Techniques: In Vitro, Expressing, Quantitative RT-PCR, Western Blot, Knockdown, Transfection, Plasmid Preparation, MTT Assay, Over Expression, Flow Cytometry, Control

NTRK2 reduces the response of LUAD cells to paclitaxel in vitro. NTRK2-knockdown A549 and A549/Taxol cells (A), NTRK2-overexpressing A549 and PC9 cells (B) as well as control cells were subjected to dose-dependent paclitaxel treatment for 48 h. The cell viability was assessed via MTT assay, and the Reed-Muench method was adopted to calculate IC 50 values. (C) The cells with NTRK2 knockdown or overexpression mentioned above and their control cells were subjected to treatment with paclitaxel at indicated concentrations for a duration of 4 days or treatment with DMSO. MTT assays were conducted to evaluate the time-dependent proliferation of these cells. Data are shown as mean ± SD. Statistical analysis was performed by two-way ANOVA. NTRK2-knockdown A549/Taxol (D) and NTRK2-overexpressing A549 cells (E) were treated with paclitaxel at indicated concentrations to evaluate the effect of NTRK2 expression on the inhibitory effect of paclitaxel on clone formation. A549/Taxol cells with NTRK2 knockdown were treated with paclitaxel or DMSO for 24 h, and cell cycle distributions (F) and apoptosis (G) were analyzed by the flow cytometry. ** P < 0.01; *** P < 0.001.

Journal: Translational Oncology

Article Title: NTRK2 promotes malignant progression and paclitaxel resistance of lung adenocarcinoma through targeting MYC/ABCF1 axis

doi: 10.1016/j.tranon.2025.102655

Figure Lengend Snippet: NTRK2 reduces the response of LUAD cells to paclitaxel in vitro. NTRK2-knockdown A549 and A549/Taxol cells (A), NTRK2-overexpressing A549 and PC9 cells (B) as well as control cells were subjected to dose-dependent paclitaxel treatment for 48 h. The cell viability was assessed via MTT assay, and the Reed-Muench method was adopted to calculate IC 50 values. (C) The cells with NTRK2 knockdown or overexpression mentioned above and their control cells were subjected to treatment with paclitaxel at indicated concentrations for a duration of 4 days or treatment with DMSO. MTT assays were conducted to evaluate the time-dependent proliferation of these cells. Data are shown as mean ± SD. Statistical analysis was performed by two-way ANOVA. NTRK2-knockdown A549/Taxol (D) and NTRK2-overexpressing A549 cells (E) were treated with paclitaxel at indicated concentrations to evaluate the effect of NTRK2 expression on the inhibitory effect of paclitaxel on clone formation. A549/Taxol cells with NTRK2 knockdown were treated with paclitaxel or DMSO for 24 h, and cell cycle distributions (F) and apoptosis (G) were analyzed by the flow cytometry. ** P < 0.01; *** P < 0.001.

Article Snippet: Human LUAD cell lines PC9, A549 and its taxol-resistant strain A549/Taxol were purchased from Procell Life Science & Technology Co.,Ltd (Wuhan, China).

Techniques: In Vitro, Knockdown, Control, MTT Assay, Endpoint Dilution Assay, Over Expression, Expressing, Flow Cytometry

ABCF1 is a key target of NTRK2 in mediating resistance to paclitaxel in LUAD cells. The mRNA (A) and protein (B) expression levels of NTRK2 and ABCF1 in A549 and A549/Taxol cells were measured by qRT-PCR and Western blotting analysis, respectively. (C) Representative immunohistochemical staining of NTRK2 and ABCF1 in LUAD tissues (Case 1), paclitaxel-resistant LUAD tissues (Case 2) and their matched noncancerous lung tissues (MN). Scale bars: 50 μm. qRT-PCR (D) and Western blotting (E) analysis results showing the effect of NTRK2 knockdown on ABCF1 expression in A549 and A549/Taxol cell lines. qRT-PCR (F) and Western blotting (G) analysis results showing the effect of ectopic expression of NTRK2 on ABCF1 expression in A549 and PC9 cells. (H) ABCF1-knockdown A549, A549/Taxol cells and control cells were subjected to dose-dependent paclitaxel treatment for 48 h. The cell viability was assessed via MTT assay, and the Reed-Muench method was adopted to calculate IC 50 values. (I) Knockdown of ABCF1 in A549 cells cooperated with overexpressing NTRK2 and their control cells were subjected to 0, 5 and 10 nM paclitaxel treatment for 48 h. The relative cell viability was assessed by MTT assay. β-actin served as an internal control for qRT-PCR. GAPDH was the internal reference for Western blotting. Data are expressed as mean ± SD. All above experiments were independently repeated in triplicate. * P < 0.05; ** P < 0.01; *** P < 0.001.

Journal: Translational Oncology

Article Title: NTRK2 promotes malignant progression and paclitaxel resistance of lung adenocarcinoma through targeting MYC/ABCF1 axis

doi: 10.1016/j.tranon.2025.102655

Figure Lengend Snippet: ABCF1 is a key target of NTRK2 in mediating resistance to paclitaxel in LUAD cells. The mRNA (A) and protein (B) expression levels of NTRK2 and ABCF1 in A549 and A549/Taxol cells were measured by qRT-PCR and Western blotting analysis, respectively. (C) Representative immunohistochemical staining of NTRK2 and ABCF1 in LUAD tissues (Case 1), paclitaxel-resistant LUAD tissues (Case 2) and their matched noncancerous lung tissues (MN). Scale bars: 50 μm. qRT-PCR (D) and Western blotting (E) analysis results showing the effect of NTRK2 knockdown on ABCF1 expression in A549 and A549/Taxol cell lines. qRT-PCR (F) and Western blotting (G) analysis results showing the effect of ectopic expression of NTRK2 on ABCF1 expression in A549 and PC9 cells. (H) ABCF1-knockdown A549, A549/Taxol cells and control cells were subjected to dose-dependent paclitaxel treatment for 48 h. The cell viability was assessed via MTT assay, and the Reed-Muench method was adopted to calculate IC 50 values. (I) Knockdown of ABCF1 in A549 cells cooperated with overexpressing NTRK2 and their control cells were subjected to 0, 5 and 10 nM paclitaxel treatment for 48 h. The relative cell viability was assessed by MTT assay. β-actin served as an internal control for qRT-PCR. GAPDH was the internal reference for Western blotting. Data are expressed as mean ± SD. All above experiments were independently repeated in triplicate. * P < 0.05; ** P < 0.01; *** P < 0.001.

Article Snippet: Human LUAD cell lines PC9, A549 and its taxol-resistant strain A549/Taxol were purchased from Procell Life Science & Technology Co.,Ltd (Wuhan, China).

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Immunohistochemical staining, Staining, Knockdown, Control, MTT Assay, Endpoint Dilution Assay

NTRK2 increases ABCF1 expression through MYC. (A) Western blotting analysis showing the effect of NTRK2 knockdown on the activity of PI3K/AKT and MAPK/ERK pathways and MYC expression in A549, A549/Taxol and PC9 cells. (B) The effect of NTRK2 overexpression on the activity of PI3K/AKT and MAPK/ERK pathways and MYC expression in A549 and PC9 cells. The effect of MYC inhibitor 10058-F4 on cell proliferation (C) and colony formation (D) of A549 cells cooperated with overexpressing NTRK2 . (E) Analysis the correlation between MYC and ABCF1 in lung cancer tissues (the data from TCGA and GTEx datasets). A549 and PC9 cells were treated with 60 μM 10058-F4 or DMSO for 24 h, and the mRNA (F) and protein (G) expression of MYC and ABCF1 were detected. A549 and PC9 cells were transfected with an empty vector (Vector) or an MYC-overexpressing plasmid (oe-MYC), the mRNA (H) and protein (I) expression levels of MYC and ABCF1 were determined by qRT-PCR and Western blotting assays. (J) The impact of MYC overexpression on the promoter activity of the wild-type (WT) and mutant (Mut) ABCF1 was evaluated using a luciferase reporter system in A549 and PC9 cells. ABCF1-Luc reporter activity was normalized to Renilla activity (Luc/Renilla). The Luc/Renilla activity was represented as means ± SD (n = 3). (K) ChIP-qPCR assay shows MYC binding to three different regions of ABCF1 promoter in A549 and PC9 cells ( n = 3). (L) qRT-PCR assay was performed to detect the mRNA expression of both MYC (left panel) and ABCF1 (right panel) in NTRK2-overexpressed cells after treating with 10058-F4 or DMSO. (M) Western blotting analysis of NTRK2, MYC and ABCF1 in NTRK2-overexpressed A549 and PC9 cells treated with 60 μM 10058-F4. β-actin was the normalized control for qRT-PCR and GAPDH served as the internal reference for Western blotting analysis. Data are shown as the mean ± SD. All above experiments were independently repeated in triplicate. ** P < 0.01; *** P < 0.001.

Journal: Translational Oncology

Article Title: NTRK2 promotes malignant progression and paclitaxel resistance of lung adenocarcinoma through targeting MYC/ABCF1 axis

doi: 10.1016/j.tranon.2025.102655

Figure Lengend Snippet: NTRK2 increases ABCF1 expression through MYC. (A) Western blotting analysis showing the effect of NTRK2 knockdown on the activity of PI3K/AKT and MAPK/ERK pathways and MYC expression in A549, A549/Taxol and PC9 cells. (B) The effect of NTRK2 overexpression on the activity of PI3K/AKT and MAPK/ERK pathways and MYC expression in A549 and PC9 cells. The effect of MYC inhibitor 10058-F4 on cell proliferation (C) and colony formation (D) of A549 cells cooperated with overexpressing NTRK2 . (E) Analysis the correlation between MYC and ABCF1 in lung cancer tissues (the data from TCGA and GTEx datasets). A549 and PC9 cells were treated with 60 μM 10058-F4 or DMSO for 24 h, and the mRNA (F) and protein (G) expression of MYC and ABCF1 were detected. A549 and PC9 cells were transfected with an empty vector (Vector) or an MYC-overexpressing plasmid (oe-MYC), the mRNA (H) and protein (I) expression levels of MYC and ABCF1 were determined by qRT-PCR and Western blotting assays. (J) The impact of MYC overexpression on the promoter activity of the wild-type (WT) and mutant (Mut) ABCF1 was evaluated using a luciferase reporter system in A549 and PC9 cells. ABCF1-Luc reporter activity was normalized to Renilla activity (Luc/Renilla). The Luc/Renilla activity was represented as means ± SD (n = 3). (K) ChIP-qPCR assay shows MYC binding to three different regions of ABCF1 promoter in A549 and PC9 cells ( n = 3). (L) qRT-PCR assay was performed to detect the mRNA expression of both MYC (left panel) and ABCF1 (right panel) in NTRK2-overexpressed cells after treating with 10058-F4 or DMSO. (M) Western blotting analysis of NTRK2, MYC and ABCF1 in NTRK2-overexpressed A549 and PC9 cells treated with 60 μM 10058-F4. β-actin was the normalized control for qRT-PCR and GAPDH served as the internal reference for Western blotting analysis. Data are shown as the mean ± SD. All above experiments were independently repeated in triplicate. ** P < 0.01; *** P < 0.001.

Article Snippet: Human LUAD cell lines PC9, A549 and its taxol-resistant strain A549/Taxol were purchased from Procell Life Science & Technology Co.,Ltd (Wuhan, China).

Techniques: Expressing, Western Blot, Knockdown, Activity Assay, Over Expression, Transfection, Plasmid Preparation, Quantitative RT-PCR, Mutagenesis, Luciferase, ChIP-qPCR, Binding Assay, Control

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