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(A) IGV snapshot of eCLIP-seq data showing binding sites and enrichment of U2AF2 and U2AF1 on the PURPL transcripts around intron 2. eCLIP-seq data for PTBP1, PRPF8, and SRSF1 are indicated. The annotated locus by RefSeq is also indicated. eCLIP data-seq was downloaded from encodeproject.org. (B) RT-qPCR after RNA-IPs using a U2AF2 antibody with primer pairs specifically detecting PURPL transcripts as indicated in Figure S1C. U2AF2 binds to transcripts containing intron 2 but not the ones with intron 1, intron 3, or spliced exons 2 and 3. Samples were normalized to IgG-IP. 18S was used as a loading control. (C) Top panel: Gel with RT-PCR products for PURPL upon knockdown of U2AF2 with 2 different siRNAs in <t>SKHEP1</t> cells. The schematics next to the gel indicate the expected products of the intron-retained and spliced isoforms. Between the two expected PCR products, we observed an extra band corresponding to the inclusion of an alternative exon inside PURPL intron 2 as observed in RefSeq, the inclusion of which is not affected by U2AF2. Quantitation of the gel bands is shown in the graphs on the right. Bottom panel: Schematic of the PCR primer triplet used to detect intron 2 retention (red) or splicing (purple). The length for each PCR product is indicated. (D) RNA-FISH images for PURPL with intron 2 retention and MALAT1 in HCT116 cells without treatment or after 24 hr of 2 mM of Hydorxyurea (HU) to induce PURPL expression. Scale bar is 10μm. (E) RT-qPCR for intron 2-containing PURPL transcript after 48 hr of 1μg/ml doxycycline treatment in comparison to no treatment in SKHEP1 PURPL -CRISPRi populations using 3 different gRNAs. (F) Proliferation assay showing the effect of overexpression of intron 2-containing PURPL transcript in the proliferation of SKHEP1 cells where the endogenous PURPL is knocked down with CRISPRi. The graph depicts the average of 3 populations with different gRNAs. The cells were treated with 1ug/ml doxycycline to induce intron 2-retained PURPL expression and cell proliferation was monitored at 3 and 6 days. Error bars represent standard deviations from 2 (E,) and 3 (C) experiments. **p<0.01, ***p<0.001.

Skhep1, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1620 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Non-canonical function of the splicing activator U2AF2 in promoting intron retention in the lncRNAs PURPL and MALAT1"

Article Title: Non-canonical function of the splicing activator U2AF2 in promoting intron retention in the lncRNAs PURPL and MALAT1

Journal: bioRxiv

doi: 10.64898/2026.02.19.706780

Figure Legend Snippet: (A) IGV snapshot of eCLIP-seq data showing binding sites and enrichment of U2AF2 and U2AF1 on the PURPL transcripts around intron 2. eCLIP-seq data for PTBP1, PRPF8, and SRSF1 are indicated. The annotated locus by RefSeq is also indicated. eCLIP data-seq was downloaded from encodeproject.org. (B) RT-qPCR after RNA-IPs using a U2AF2 antibody with primer pairs specifically detecting PURPL transcripts as indicated in Figure S1C. U2AF2 binds to transcripts containing intron 2 but not the ones with intron 1, intron 3, or spliced exons 2 and 3. Samples were normalized to IgG-IP. 18S was used as a loading control. (C) Top panel: Gel with RT-PCR products for PURPL upon knockdown of U2AF2 with 2 different siRNAs in SKHEP1 cells. The schematics next to the gel indicate the expected products of the intron-retained and spliced isoforms. Between the two expected PCR products, we observed an extra band corresponding to the inclusion of an alternative exon inside PURPL intron 2 as observed in RefSeq, the inclusion of which is not affected by U2AF2. Quantitation of the gel bands is shown in the graphs on the right. Bottom panel: Schematic of the PCR primer triplet used to detect intron 2 retention (red) or splicing (purple). The length for each PCR product is indicated. (D) RNA-FISH images for PURPL with intron 2 retention and MALAT1 in HCT116 cells without treatment or after 24 hr of 2 mM of Hydorxyurea (HU) to induce PURPL expression. Scale bar is 10μm. (E) RT-qPCR for intron 2-containing PURPL transcript after 48 hr of 1μg/ml doxycycline treatment in comparison to no treatment in SKHEP1 PURPL -CRISPRi populations using 3 different gRNAs. (F) Proliferation assay showing the effect of overexpression of intron 2-containing PURPL transcript in the proliferation of SKHEP1 cells where the endogenous PURPL is knocked down with CRISPRi. The graph depicts the average of 3 populations with different gRNAs. The cells were treated with 1ug/ml doxycycline to induce intron 2-retained PURPL expression and cell proliferation was monitored at 3 and 6 days. Error bars represent standard deviations from 2 (E,) and 3 (C) experiments. **p<0.01, ***p<0.001.

Techniques Used: Binding Assay, Quantitative RT-PCR, Control, Reverse Transcription Polymerase Chain Reaction, Knockdown, Quantitation Assay, Expressing, Comparison, Proliferation Assay, Over Expression

(A) U2AF2 was knocked down in SKHEP1 cells and 72 hr later, RNA was extracted and RNA-seq was performed. Left : Number of decreased (blue) and increased (red) IR events at various p-values after U2AF2 knockdown as analyzed with the IR Finder algorithm. The purple arrow indicates the PURPL IR event and green arrows indicate MALAT IR events Right : Pie chart of the numbers of increased and decreased IR events upon U2AF2 knockdown. (B) Floating bar plot showing the IR ratio of PURPL intron 2 and the IR ratio of intron 1 (middle) and intron 2 (right) of MALAT1 . siCTRL and siU2AF2#1 samples as analyzed with the IRFinder algorithm. (C) and (E) RT-PCR for MALAT1 using a primer pair flanking the regulated intron 1 (C) or intron 2 (E) upon knockdown of U2AF2 with 2 different siRNAs in HCT116 and SKHEP1 cells. The schematics next to the gel indicate the expected products of the intron-retained and spliced isoforms. (D) and (F) Bar graph with quantitation of the gel bands from (C) and (E) in SKHEP1 cells. Error bars represent standard deviations from 2 independent experiments. *p<0.05, **p<0.01, ***p<0.001.

Figure Legend Snippet: (A) U2AF2 was knocked down in SKHEP1 cells and 72 hr later, RNA was extracted and RNA-seq was performed. Left : Number of decreased (blue) and increased (red) IR events at various p-values after U2AF2 knockdown as analyzed with the IR Finder algorithm. The purple arrow indicates the PURPL IR event and green arrows indicate MALAT IR events Right : Pie chart of the numbers of increased and decreased IR events upon U2AF2 knockdown. (B) Floating bar plot showing the IR ratio of PURPL intron 2 and the IR ratio of intron 1 (middle) and intron 2 (right) of MALAT1 . siCTRL and siU2AF2#1 samples as analyzed with the IRFinder algorithm. (C) and (E) RT-PCR for MALAT1 using a primer pair flanking the regulated intron 1 (C) or intron 2 (E) upon knockdown of U2AF2 with 2 different siRNAs in HCT116 and SKHEP1 cells. The schematics next to the gel indicate the expected products of the intron-retained and spliced isoforms. (D) and (F) Bar graph with quantitation of the gel bands from (C) and (E) in SKHEP1 cells. Error bars represent standard deviations from 2 independent experiments. *p<0.05, **p<0.01, ***p<0.001.

Techniques Used: RNA Sequencing, Knockdown, Reverse Transcription Polymerase Chain Reaction, Quantitation Assay

(A) RNA-FISH images for MALAT1 and Immunofluorescence images for SON is shown upon transfection of SKHEP1 cells with siCTRL or siU2AF2. MALAT1 is enriched in nuclear speckles in the siCTRL but not upon U2AF2 knockdown. (B) Quantitation of the speckle to nuclear plasma MALAT1 signal ratio in the three replicates in panel (A) . ****p<0.0001.

Figure Legend Snippet: (A) RNA-FISH images for MALAT1 and Immunofluorescence images for SON is shown upon transfection of SKHEP1 cells with siCTRL or siU2AF2. MALAT1 is enriched in nuclear speckles in the siCTRL but not upon U2AF2 knockdown. (B) Quantitation of the speckle to nuclear plasma MALAT1 signal ratio in the three replicates in panel (A) . ****p<0.0001.

Techniques Used: Immunofluorescence, Transfection, Knockdown, Quantitation Assay, Clinical Proteomics

Isolation:

Article Title: Imaging and targeting S1PR1 in HER2+ tumors
Article Snippet: .. NCIN87 (human gastric cancer cells, RRID:CVCL 1603) and SKHEP1 (endothelial cells that were isolated from the liver of a patient with adenocarcinoma, RRID:CVCL_0525) were purchased from the American Type Culture Collection. ..

Article Title: Imaging and targeting S1PR1 in HER2+ tumors.
Article Snippet: Human Epidermal Growth Factor Receptor 2 (HER2) is a membrane receptor tyrosine kinase overexpressed in a subset of gastric cancers and is the target of multiple clinically approved therapies, including the antibody-drug conjugate trastuzumab deruxtecan (T-DXd).. However, resistance to HER2-directed therapies remains a major challenge in gastric cancer.. Sphingosine-1-phosphate receptor 1 (S1PR1), a G-protein-coupled receptor involved in oncogenic signaling, has been associated with poor prognosis and therapy resistance.

Planar Chromatography:

Article Title: NAT10 drives hepatocellular carcinoma progression through SQLE-mediated cholesterol biosynthesis and is targetable by remodelin
Article Snippet: .. HepG2, SKHep1, and PLC/PRF/5 cells were acquired from ATCC (Manassas, VA). ..

Multiple Displacement Amplification:

Article Title: Non-canonical function of the splicing activator U2AF2 in promoting intron retention in the lncRNAs PURPL and MALAT1
Article Snippet: .. HAP1, HCT116, HEK293T, HepG2, RPE1, SKHEP1, U2OS, WI38, and MDA-MB-231 cells were purchased from ATCC and maintained in Dulbecco’s Modified Eagle Medium (DMEM) (Gibco) supplemented with 10% (v/v) fetal bovine serum (Gibco) and 1% (v/v) PenStrep (Gibco) in a 5% CO 2 atmosphere at 37°C. .. All cell lines were routinely confirmed to be free of mycoplasma using Venor GeM Mycoplasma Detection Kit (Millipore Sigma-Aldrich).

Modification:

Image Search Results

Journal: bioRxiv

Article Title: Non-canonical function of the splicing activator U2AF2 in promoting intron retention in the lncRNAs PURPL and MALAT1

doi: 10.64898/2026.02.19.706780

Figure Lengend Snippet: (A) IGV snapshot of eCLIP-seq data showing binding sites and enrichment of U2AF2 and U2AF1 on the PURPL transcripts around intron 2. eCLIP-seq data for PTBP1, PRPF8, and SRSF1 are indicated. The annotated locus by RefSeq is also indicated. eCLIP data-seq was downloaded from encodeproject.org. (B) RT-qPCR after RNA-IPs using a U2AF2 antibody with primer pairs specifically detecting PURPL transcripts as indicated in Figure S1C. U2AF2 binds to transcripts containing intron 2 but not the ones with intron 1, intron 3, or spliced exons 2 and 3. Samples were normalized to IgG-IP. 18S was used as a loading control. (C) Top panel: Gel with RT-PCR products for PURPL upon knockdown of U2AF2 with 2 different siRNAs in SKHEP1 cells. The schematics next to the gel indicate the expected products of the intron-retained and spliced isoforms. Between the two expected PCR products, we observed an extra band corresponding to the inclusion of an alternative exon inside PURPL intron 2 as observed in RefSeq, the inclusion of which is not affected by U2AF2. Quantitation of the gel bands is shown in the graphs on the right. Bottom panel: Schematic of the PCR primer triplet used to detect intron 2 retention (red) or splicing (purple). The length for each PCR product is indicated. (D) RNA-FISH images for PURPL with intron 2 retention and MALAT1 in HCT116 cells without treatment or after 24 hr of 2 mM of Hydorxyurea (HU) to induce PURPL expression. Scale bar is 10μm. (E) RT-qPCR for intron 2-containing PURPL transcript after 48 hr of 1μg/ml doxycycline treatment in comparison to no treatment in SKHEP1 PURPL -CRISPRi populations using 3 different gRNAs. (F) Proliferation assay showing the effect of overexpression of intron 2-containing PURPL transcript in the proliferation of SKHEP1 cells where the endogenous PURPL is knocked down with CRISPRi. The graph depicts the average of 3 populations with different gRNAs. The cells were treated with 1ug/ml doxycycline to induce intron 2-retained PURPL expression and cell proliferation was monitored at 3 and 6 days. Error bars represent standard deviations from 2 (E,) and 3 (C) experiments. **p<0.01, ***p<0.001.

Article Snippet: HAP1, HCT116, HEK293T, HepG2, RPE1, SKHEP1, U2OS, WI38, and MDA-MB-231 cells were purchased from ATCC and maintained in Dulbecco’s Modified Eagle Medium (DMEM) (Gibco) supplemented with 10% (v/v) fetal bovine serum (Gibco) and 1% (v/v) PenStrep (Gibco) in a 5% CO 2 atmosphere at 37°C.

Techniques: Binding Assay, Quantitative RT-PCR, Control, Reverse Transcription Polymerase Chain Reaction, Knockdown, Quantitation Assay, Expressing, Comparison, Proliferation Assay, Over Expression

Journal: bioRxiv

Article Title: Non-canonical function of the splicing activator U2AF2 in promoting intron retention in the lncRNAs PURPL and MALAT1

doi: 10.64898/2026.02.19.706780

Figure Lengend Snippet: (A) U2AF2 was knocked down in SKHEP1 cells and 72 hr later, RNA was extracted and RNA-seq was performed. Left : Number of decreased (blue) and increased (red) IR events at various p-values after U2AF2 knockdown as analyzed with the IR Finder algorithm. The purple arrow indicates the PURPL IR event and green arrows indicate MALAT IR events Right : Pie chart of the numbers of increased and decreased IR events upon U2AF2 knockdown. (B) Floating bar plot showing the IR ratio of PURPL intron 2 and the IR ratio of intron 1 (middle) and intron 2 (right) of MALAT1 . siCTRL and siU2AF2#1 samples as analyzed with the IRFinder algorithm. (C) and (E) RT-PCR for MALAT1 using a primer pair flanking the regulated intron 1 (C) or intron 2 (E) upon knockdown of U2AF2 with 2 different siRNAs in HCT116 and SKHEP1 cells. The schematics next to the gel indicate the expected products of the intron-retained and spliced isoforms. (D) and (F) Bar graph with quantitation of the gel bands from (C) and (E) in SKHEP1 cells. Error bars represent standard deviations from 2 independent experiments. *p<0.05, **p<0.01, ***p<0.001.

Techniques: RNA Sequencing, Knockdown, Reverse Transcription Polymerase Chain Reaction, Quantitation Assay

Journal: bioRxiv

Article Title: Non-canonical function of the splicing activator U2AF2 in promoting intron retention in the lncRNAs PURPL and MALAT1

doi: 10.64898/2026.02.19.706780

Figure Lengend Snippet: (A) RNA-FISH images for MALAT1 and Immunofluorescence images for SON is shown upon transfection of SKHEP1 cells with siCTRL or siU2AF2. MALAT1 is enriched in nuclear speckles in the siCTRL but not upon U2AF2 knockdown. (B) Quantitation of the speckle to nuclear plasma MALAT1 signal ratio in the three replicates in panel (A) . ****p<0.0001.

Techniques: Immunofluorescence, Transfection, Knockdown, Quantitation Assay, Clinical Proteomics

NAT10 knockdown suppresses cell proliferation in HCC cell lines (A) Western blot analysis of NAT10 and PCNA in MHCC97H, SKHep1, and HepG2 cells with knockdown of NAT10. (B–D) The effects of NAT10 knockdown on cell growth (B), colony formation (C), and wound healing (D) ( n = 3, performed in triplicate). (E and F) Effects of NAT10 re-expression on cell growth (E) and colony formation (F) in SKHep1-sgNAT10 and MHCC97H-sgNAT10 cells. ( n = 3, performed in triplicate). Data are represented as means ± SD. Unpaired, two-tailed Student’s t test (C, D, and F). Difference in cell viability between two groups was determined by repeated-measures ANOVA (B, E) ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Journal: iScience

Article Title: NAT10 drives hepatocellular carcinoma progression through SQLE-mediated cholesterol biosynthesis and is targetable by remodelin

doi: 10.1016/j.isci.2025.114488

Figure Lengend Snippet: NAT10 knockdown suppresses cell proliferation in HCC cell lines (A) Western blot analysis of NAT10 and PCNA in MHCC97H, SKHep1, and HepG2 cells with knockdown of NAT10. (B–D) The effects of NAT10 knockdown on cell growth (B), colony formation (C), and wound healing (D) ( n = 3, performed in triplicate). (E and F) Effects of NAT10 re-expression on cell growth (E) and colony formation (F) in SKHep1-sgNAT10 and MHCC97H-sgNAT10 cells. ( n = 3, performed in triplicate). Data are represented as means ± SD. Unpaired, two-tailed Student’s t test (C, D, and F). Difference in cell viability between two groups was determined by repeated-measures ANOVA (B, E) ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: Human: SKHep1 cells , ATCC , HTB-52; RRID: CVCL_0525.

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

NAT10 contributes to HCC development in vivo (A and B) Subcutaneous tumors derived from MHCC97H cells with NAT10 knockout analyzed for tumor weight and volume (A), H&E staining, Ki-67 staining, and PCNA staining in subcutaneous tumors derived from MHCC97H cells with NAT10 knockout (B) ( n = 10). (C) Western blots analysis of NAT10 and PCNA expression in subcutaneous tumors derived from MHCC97H cells with NAT10 knockout. (D–F) Subcutaneous tumors derived from SKHep1 cells with NAT10 knockout analyzed for tumor weight and volume (D), H&E staining, Ki-67 staining, and PCNA staining in subcutaneous tumors derived from SKHep1 cells with NAT10 knockout (E) and PCNA protein expression (F) ( n = 8 for sgControl and n = 10 for sgNAT10). (G and H) Subcutaneous tumors derived from NAT10-overexpressing MHCC97H cells were analyzed for tumor weight and volume (G), H&E staining, Ki-67 staining, and PCNA staining in subcutaneous tumors derived from NAT10-overexpressing MHCC97H cells (H) ( n = 8). (I) Western blots analysis of NAT10 and PCNA expression in subcutaneous tumors derived from NAT10-overexpressing MHCC97H cells. Data are represented as means ± SD. Unpaired, two-tailed Student’s t test (A [middle], B, D [middle], E, G [middle], H). Difference in tumor volume between two groups was determined by repeated-measures ANOVA (A [right], D [right], G [right]). Scale bars, 200 μm (B, E, H). ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Journal: iScience

Article Title: NAT10 drives hepatocellular carcinoma progression through SQLE-mediated cholesterol biosynthesis and is targetable by remodelin

doi: 10.1016/j.isci.2025.114488

Figure Lengend Snippet: NAT10 contributes to HCC development in vivo (A and B) Subcutaneous tumors derived from MHCC97H cells with NAT10 knockout analyzed for tumor weight and volume (A), H&E staining, Ki-67 staining, and PCNA staining in subcutaneous tumors derived from MHCC97H cells with NAT10 knockout (B) ( n = 10). (C) Western blots analysis of NAT10 and PCNA expression in subcutaneous tumors derived from MHCC97H cells with NAT10 knockout. (D–F) Subcutaneous tumors derived from SKHep1 cells with NAT10 knockout analyzed for tumor weight and volume (D), H&E staining, Ki-67 staining, and PCNA staining in subcutaneous tumors derived from SKHep1 cells with NAT10 knockout (E) and PCNA protein expression (F) ( n = 8 for sgControl and n = 10 for sgNAT10). (G and H) Subcutaneous tumors derived from NAT10-overexpressing MHCC97H cells were analyzed for tumor weight and volume (G), H&E staining, Ki-67 staining, and PCNA staining in subcutaneous tumors derived from NAT10-overexpressing MHCC97H cells (H) ( n = 8). (I) Western blots analysis of NAT10 and PCNA expression in subcutaneous tumors derived from NAT10-overexpressing MHCC97H cells. Data are represented as means ± SD. Unpaired, two-tailed Student’s t test (A [middle], B, D [middle], E, G [middle], H). Difference in tumor volume between two groups was determined by repeated-measures ANOVA (A [right], D [right], G [right]). Scale bars, 200 μm (B, E, H). ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: Human: SKHep1 cells , ATCC , HTB-52; RRID: CVCL_0525.

Techniques: In Vivo, Derivative Assay, Knock-Out, Staining, Western Blot, Expressing, Two Tailed Test

Increased cholesterol level mediates NAT10 function in HCC progression (A) Intracellular cholesterol levels in MHCC97H, SKHep1, and HepG2 cells overexpressing NAT10 or NAT10 knockout (sgNAT10) in MHCC97H, SKHep1, and HepG2 cells ( n = 3, performed in triplicate). (B and C) Cholesterol supplementation restored proliferation (B) and colony formation (C) in SKHep1-sgNAT10 and MHCC97H-sgNAT10 cells. ( n = 3, performed in triplicate). (D and E) A high-cholesterol diet (HCD) restored tumor growth in tumor-bearing mice with subcutaneously inoculated SKHep1-sgNAT10 xenografts and eliminated the antitumor effect of NAT10 knockout ( n = 6 for control and n = 8 for cholesterol). Data represent mean ± SD; unpaired, two-tailed Student’s t test (C, D) or two-way ANOVA (B, E). The significance of the difference in cholesterol concentrations was determined by Mann-Whitney U test (A). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Journal: iScience

Article Title: NAT10 drives hepatocellular carcinoma progression through SQLE-mediated cholesterol biosynthesis and is targetable by remodelin

doi: 10.1016/j.isci.2025.114488

Figure Lengend Snippet: Increased cholesterol level mediates NAT10 function in HCC progression (A) Intracellular cholesterol levels in MHCC97H, SKHep1, and HepG2 cells overexpressing NAT10 or NAT10 knockout (sgNAT10) in MHCC97H, SKHep1, and HepG2 cells ( n = 3, performed in triplicate). (B and C) Cholesterol supplementation restored proliferation (B) and colony formation (C) in SKHep1-sgNAT10 and MHCC97H-sgNAT10 cells. ( n = 3, performed in triplicate). (D and E) A high-cholesterol diet (HCD) restored tumor growth in tumor-bearing mice with subcutaneously inoculated SKHep1-sgNAT10 xenografts and eliminated the antitumor effect of NAT10 knockout ( n = 6 for control and n = 8 for cholesterol). Data represent mean ± SD; unpaired, two-tailed Student’s t test (C, D) or two-way ANOVA (B, E). The significance of the difference in cholesterol concentrations was determined by Mann-Whitney U test (A). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: Human: SKHep1 cells , ATCC , HTB-52; RRID: CVCL_0525.

Techniques: Knock-Out, Control, Two Tailed Test, MANN-WHITNEY

NAT10 promotes HCC progression via cholesterol biosynthesis and SQLE/AKT/mTOR signaling (A) KEGG pathway analysis of the RNA-Seq data derived from subcutaneous tumor tissues with NAT10 knockdown relative to a control vector. GSEA of the RNA-Seq data from subcutaneous tumor tissues with NAT10 knockdown relative to a control vector. (B) Elevated NAT10 expression in HCC patients correlates with enhanced cholesterol biosynthesis pathway scores in the ICGC cohort ( p < 0.0001 ) ( n = 101 for low and n = 102 for high) and the OEP000321 (Fudan University) protein database ( p < 0.05 ). ( n = 79 for low and n = 80 for high). (C and D) NAT10 knockout (sgNAT10) reduces mRNA (C) and protein (D) levels of cholesterol biosynthesis genes (SQLE, LSS, and DHCR24) in liver cancer cells, while NAT10 overexpression increases SQLE and LSS protein expression in MHCC97H cells (see A–S4C for expanded profiles). (E and F) Overexpression of SQLE rescues cell viability (E) and colony formation (F) ( n = 3, performed in triplicate) in SKHep1-sgNAT10 and MHCC97H-sgNAT10 cells. (G and H) Terbinafine (SQLE inhibitor) exhibits anti-proliferative effects comparable to NAT10 knockout and synergistically reduces HCC cell viability when combined with sgNAT10 ( n = 3, performed in triplicate). (I and J) NAT10 regulates SQLE activation through the AKT/mTOR pathway, as demonstrated by modulating mTOR expression. Data represent mean ± SD; unpaired, two-tailed Student’s t test (B, F, H) or ANOVA with repeated-measures analysis of variance two-way ANOVA (E, G). Mann-Whitney U test was used to assess the significance of the differences in mRNA expression (C). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Journal: iScience

Article Title: NAT10 drives hepatocellular carcinoma progression through SQLE-mediated cholesterol biosynthesis and is targetable by remodelin

doi: 10.1016/j.isci.2025.114488

Figure Lengend Snippet: NAT10 promotes HCC progression via cholesterol biosynthesis and SQLE/AKT/mTOR signaling (A) KEGG pathway analysis of the RNA-Seq data derived from subcutaneous tumor tissues with NAT10 knockdown relative to a control vector. GSEA of the RNA-Seq data from subcutaneous tumor tissues with NAT10 knockdown relative to a control vector. (B) Elevated NAT10 expression in HCC patients correlates with enhanced cholesterol biosynthesis pathway scores in the ICGC cohort ( p < 0.0001 ) ( n = 101 for low and n = 102 for high) and the OEP000321 (Fudan University) protein database ( p < 0.05 ). ( n = 79 for low and n = 80 for high). (C and D) NAT10 knockout (sgNAT10) reduces mRNA (C) and protein (D) levels of cholesterol biosynthesis genes (SQLE, LSS, and DHCR24) in liver cancer cells, while NAT10 overexpression increases SQLE and LSS protein expression in MHCC97H cells (see A–S4C for expanded profiles). (E and F) Overexpression of SQLE rescues cell viability (E) and colony formation (F) ( n = 3, performed in triplicate) in SKHep1-sgNAT10 and MHCC97H-sgNAT10 cells. (G and H) Terbinafine (SQLE inhibitor) exhibits anti-proliferative effects comparable to NAT10 knockout and synergistically reduces HCC cell viability when combined with sgNAT10 ( n = 3, performed in triplicate). (I and J) NAT10 regulates SQLE activation through the AKT/mTOR pathway, as demonstrated by modulating mTOR expression. Data represent mean ± SD; unpaired, two-tailed Student’s t test (B, F, H) or ANOVA with repeated-measures analysis of variance two-way ANOVA (E, G). Mann-Whitney U test was used to assess the significance of the differences in mRNA expression (C). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: Human: SKHep1 cells , ATCC , HTB-52; RRID: CVCL_0525.

Techniques: RNA Sequencing, Derivative Assay, Knockdown, Control, Plasmid Preparation, Expressing, Knock-Out, Over Expression, Activation Assay, Two Tailed Test, MANN-WHITNEY

Pharmacological inhibition of NAT10 suppresses HCC progression in vitro and in vivo (A) Western blot analysis showing reduced NAT10 protein levels in MHCC97H, PLC/PRF/5, SKHep1, and HepG2 cells treated with remodelin. (B) The mRNA levels of cholesterol biosynthesis genes (including SQLE, LSS, DHCR24, PMVK, HMGCR, SC4MOL, and SC5D) in remodelin-treated MHCC97H, SKHep1, and PLC/PRF/5 cells ( n = 3, performed in triplicate). (C) Cholesterol levels in remodelin-treated MHCC97H, SKHep1, and PLC/PRF/5 cells ( n = 3, performed in triplicate). (D and E) Remodelin treatment significantly inhibited cell viability (D) and colony formation (E) in multiple HCC cell lines ( n = 3, performed in triplicate). (F and G) Remodelin failed to suppress cell growth (F) or colony formation (G) in NAT10-knockout (sgNAT10) HCC cells, indicating NAT10-dependent anti-proliferative effects ( n = 3, performed in triplicate). (H) Remodelin administration (60 mg/kg/day, oral gavage) suppressed tumor growth in subcutaneous SKHep1 xenograft models, as evidenced by reduced tumor size and weight ( p < 0.001) ( n = 10). (I) H&E staining, Ki-67 staining and in subcutaneous tumors derived from remodelin-treated SKHep1 cells. (J) Western blots analysis of NAT10 and PCNA expression in subcutaneous tumors derived from remodelin-treated SKHep1 cells. (K) Remodelin administration (60 mg/kg/day, oral gavage) suppressed tumor growth in subcutaneous MHCC97H xenograft models, as evidenced by reduced tumor size and weight ( p < 0.001) ( n = 8). (L) H&E staining, Ki-67 staining and in subcutaneous tumors derived from remodelin-treated MHCC97H cells. (M) Western blots analysis of NAT10 and PCNA expression in subcutaneous tumors derived from remodelin-treated MHCC97H cells. Data are represented as means ± SD. Unpaired, two-tailed Student’s t test (E, G, H [middle], I, K [middle], and L). Difference between two groups was determined by repeated-measures ANOVA (D, F, H [right], K [right]). Mann-Whitney U test was used to assess the significance of the differences in mRNA expression, cholesterol concentrations (B, C). Scale bars, 200 μm (I, L). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Journal: iScience

Article Title: NAT10 drives hepatocellular carcinoma progression through SQLE-mediated cholesterol biosynthesis and is targetable by remodelin

doi: 10.1016/j.isci.2025.114488

Figure Lengend Snippet: Pharmacological inhibition of NAT10 suppresses HCC progression in vitro and in vivo (A) Western blot analysis showing reduced NAT10 protein levels in MHCC97H, PLC/PRF/5, SKHep1, and HepG2 cells treated with remodelin. (B) The mRNA levels of cholesterol biosynthesis genes (including SQLE, LSS, DHCR24, PMVK, HMGCR, SC4MOL, and SC5D) in remodelin-treated MHCC97H, SKHep1, and PLC/PRF/5 cells ( n = 3, performed in triplicate). (C) Cholesterol levels in remodelin-treated MHCC97H, SKHep1, and PLC/PRF/5 cells ( n = 3, performed in triplicate). (D and E) Remodelin treatment significantly inhibited cell viability (D) and colony formation (E) in multiple HCC cell lines ( n = 3, performed in triplicate). (F and G) Remodelin failed to suppress cell growth (F) or colony formation (G) in NAT10-knockout (sgNAT10) HCC cells, indicating NAT10-dependent anti-proliferative effects ( n = 3, performed in triplicate). (H) Remodelin administration (60 mg/kg/day, oral gavage) suppressed tumor growth in subcutaneous SKHep1 xenograft models, as evidenced by reduced tumor size and weight ( p < 0.001) ( n = 10). (I) H&E staining, Ki-67 staining and in subcutaneous tumors derived from remodelin-treated SKHep1 cells. (J) Western blots analysis of NAT10 and PCNA expression in subcutaneous tumors derived from remodelin-treated SKHep1 cells. (K) Remodelin administration (60 mg/kg/day, oral gavage) suppressed tumor growth in subcutaneous MHCC97H xenograft models, as evidenced by reduced tumor size and weight ( p < 0.001) ( n = 8). (L) H&E staining, Ki-67 staining and in subcutaneous tumors derived from remodelin-treated MHCC97H cells. (M) Western blots analysis of NAT10 and PCNA expression in subcutaneous tumors derived from remodelin-treated MHCC97H cells. Data are represented as means ± SD. Unpaired, two-tailed Student’s t test (E, G, H [middle], I, K [middle], and L). Difference between two groups was determined by repeated-measures ANOVA (D, F, H [right], K [right]). Mann-Whitney U test was used to assess the significance of the differences in mRNA expression, cholesterol concentrations (B, C). Scale bars, 200 μm (I, L). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: Human: SKHep1 cells , ATCC , HTB-52; RRID: CVCL_0525.

Techniques: Inhibition, In Vitro, In Vivo, Western Blot, Knock-Out, Staining, Derivative Assay, Expressing, Two Tailed Test, MANN-WHITNEY

Validation of NOP56 expression and subcellular localization in HCC. (A) RT-PCR analysis of NOP56 mRNA levels in paired HCC and adjacent non-tumor tissues. (B) Western blot analysis of NOP56 protein expression in paired HCC and adjacent non-tumor tissues, with quantification on the right. (C) Representative immunohistochemical staining of NOP56 in HCC and adjacent non-tumor tissues, with H-score analysis. (D) NOP56 mRNA expression in liver cancer cell lines (PLC, HepG2, SKhep1, Huh7) and normal liver cell line (MIHA). (E) Western blot analysis of NOP56 protein expression in liver cancer cell lines and MIHA, with quantification on the right. (F) Immunofluorescence images showing predominant nucleolar localization of NOP56 in Huh7 and SKhep1 cells. Data were shown as mean ± SD. *: p < 0.05, **: p < 0.01, ***: p < 0.001.

Journal: Frontiers in Oncology

Article Title: NOP56 interacts with Fibrarin to regulate the PI3K/AKT signaling pathway and inhibit apoptosis of hepatocellular carcinoma

doi: 10.3389/fonc.2025.1728226

Figure Lengend Snippet: Validation of NOP56 expression and subcellular localization in HCC. (A) RT-PCR analysis of NOP56 mRNA levels in paired HCC and adjacent non-tumor tissues. (B) Western blot analysis of NOP56 protein expression in paired HCC and adjacent non-tumor tissues, with quantification on the right. (C) Representative immunohistochemical staining of NOP56 in HCC and adjacent non-tumor tissues, with H-score analysis. (D) NOP56 mRNA expression in liver cancer cell lines (PLC, HepG2, SKhep1, Huh7) and normal liver cell line (MIHA). (E) Western blot analysis of NOP56 protein expression in liver cancer cell lines and MIHA, with quantification on the right. (F) Immunofluorescence images showing predominant nucleolar localization of NOP56 in Huh7 and SKhep1 cells. Data were shown as mean ± SD. *: p < 0.05, **: p < 0.01, ***: p < 0.001.

Article Snippet: HepG2, Huh7, SKhep1, PLC, and the normal hepatic cell line MIHA were all purchased from Servicebio (Wuhan, China).

Techniques: Biomarker Discovery, Expressing, Reverse Transcription Polymerase Chain Reaction, Western Blot, Immunohistochemical staining, Staining, Immunofluorescence

Silencing of NOP56 suppresses proliferation, migration, and tumorigenicity of HCC cells in vitro and in vivo . (A) qRT-PCR analysis of NOP56 mRNA levels in Huh7 and SKhep1 cells transduced with control (NC) or NOP56-targeting shRNAs (Sh1, Sh2). (B) Western blot analysis of NOP56 protein levels with β-actin as a loading control; quantification shown on the right. (C) Growth curves showing reduced proliferation in NOP56-knockdown cells compared with NC. (D) Representative images and quantification of colony formation assays. (E) Wound-healing assays showing impaired migration after NOP56 knockdown. (F) Transwell migration assays confirming reduced migratory capacity. (G–H) Representative xenograft tumors, tumor volume, and weight measurements from nude mice injected with Huh7 cells expressing NC or NOP56 shRNAs. (I) Immunohistochemical staining of NOP56 and Ki-67 in xenograft tumor tissues. Data were shown as mean ± SD. *: p < 0.05, **: p < 0.01, ***: p < 0.001.

Journal: Frontiers in Oncology

Article Title: NOP56 interacts with Fibrarin to regulate the PI3K/AKT signaling pathway and inhibit apoptosis of hepatocellular carcinoma

doi: 10.3389/fonc.2025.1728226

Figure Lengend Snippet: Silencing of NOP56 suppresses proliferation, migration, and tumorigenicity of HCC cells in vitro and in vivo . (A) qRT-PCR analysis of NOP56 mRNA levels in Huh7 and SKhep1 cells transduced with control (NC) or NOP56-targeting shRNAs (Sh1, Sh2). (B) Western blot analysis of NOP56 protein levels with β-actin as a loading control; quantification shown on the right. (C) Growth curves showing reduced proliferation in NOP56-knockdown cells compared with NC. (D) Representative images and quantification of colony formation assays. (E) Wound-healing assays showing impaired migration after NOP56 knockdown. (F) Transwell migration assays confirming reduced migratory capacity. (G–H) Representative xenograft tumors, tumor volume, and weight measurements from nude mice injected with Huh7 cells expressing NC or NOP56 shRNAs. (I) Immunohistochemical staining of NOP56 and Ki-67 in xenograft tumor tissues. Data were shown as mean ± SD. *: p < 0.05, **: p < 0.01, ***: p < 0.001.

Article Snippet: HepG2, Huh7, SKhep1, PLC, and the normal hepatic cell line MIHA were all purchased from Servicebio (Wuhan, China).

Techniques: Migration, In Vitro, In Vivo, Quantitative RT-PCR, Transduction, Control, Western Blot, Knockdown, Injection, Expressing, Immunohistochemical staining, Staining

NOP56 regulates cell cycle progression and apoptosis in HCC cells. (A) Volcano plot of differentially expressed genes (DEGs) between high and low NOP56 expression groups in TCGA-LIHC; KEGG pathway enrichment analysis showing significant enrichment in cell cycle and apoptosis-related pathways. (B) Flow cytometry analysis of cell cycle distribution in Huh7 and SKhep1 cells with NOP56 knockdown, indicating G0/G1 arrest. (C) Annexin V/PI staining and quantification showing increased apoptosis after NOP56 silencing. (D) Western blot analysis of CDK1, CDK4, BCL2, and cleaved caspase-3 (C-Caspase3) expression in NOP56-depleted and control cells. Data were shown as mean ± SD. *: p < 0.05, **: p < 0.01, ***: p < 0.001.

Journal: Frontiers in Oncology

Article Title: NOP56 interacts with Fibrarin to regulate the PI3K/AKT signaling pathway and inhibit apoptosis of hepatocellular carcinoma

doi: 10.3389/fonc.2025.1728226

Figure Lengend Snippet: NOP56 regulates cell cycle progression and apoptosis in HCC cells. (A) Volcano plot of differentially expressed genes (DEGs) between high and low NOP56 expression groups in TCGA-LIHC; KEGG pathway enrichment analysis showing significant enrichment in cell cycle and apoptosis-related pathways. (B) Flow cytometry analysis of cell cycle distribution in Huh7 and SKhep1 cells with NOP56 knockdown, indicating G0/G1 arrest. (C) Annexin V/PI staining and quantification showing increased apoptosis after NOP56 silencing. (D) Western blot analysis of CDK1, CDK4, BCL2, and cleaved caspase-3 (C-Caspase3) expression in NOP56-depleted and control cells. Data were shown as mean ± SD. *: p < 0.05, **: p < 0.01, ***: p < 0.001.

Article Snippet: HepG2, Huh7, SKhep1, PLC, and the normal hepatic cell line MIHA were all purchased from Servicebio (Wuhan, China).

Techniques: Expressing, Flow Cytometry, Knockdown, Staining, Western Blot, Control

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1) Product Images from "Non-canonical function of the splicing activator U2AF2 in promoting intron retention in the lncRNAs PURPL and MALAT1"

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