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MATN1‐AS1 regulates <t>E2F2</t> expression in ccRCC. (A) Heatmap showing DEGs expression profiles of 786‐O cells transfected with control (Control 1–3) or MATN1‐AS1 targeted sequence (sh 1–3). Data were normalised with FPKM. Results were filtered with p < 0.05, |log 2 FC| > 1. (B, C) GSEA of Control and MATN1‐AS1 knocked down groups. (D) Heatmap showing the expression level changes of the E2F family after knocking down MATN1‐AS1. Data were normalised with FPKM. (E) Co‐expression analysis of E2Fs with MATN1‐AS1 in TCGA‐KIRC dataset (Pearson correlation test). (F) Expression correlation between E2F2 and MATN1‐AS1 in TCGA‐KIRC dataset (Pearson correlation test). (G) E2F2 expression levels in ccRCC and normal tissues in the TCGA‐KIRC dataset (Data were normalised with log 2 (TPM + 1), Mean ± SEM, Wilcoxon test, *** p < 0.001). (H) E2F2 expression levels in ccRCC and normal tissues in the ICGC‐RECA dataset (Data were normalised with log 2 (TPM + 1), Mean ± SEM, Wilcoxon test, *** p < 0.001). (I) Overall survival (OS) curves of E2F2 in ccRCC (Log‐rank test, * p < 0.05). (J, K) GSEA between High‐ and Low‐E2F2 expression individuals from TCGA‐KIRC dataset. (L) E2F2 expression level changes after knocking down MATN1‐AS1. (M) Potential micro‐RNA links between MATN1‐AS1 and E2F2. (N) miR‐214‐5p expression levels in ccRCC and renal tissue from TCGA‐KIRC dataset ( p = 2.2 × 10 −13 ). (O, P) Binding sites schematic diagrams of miR‐214‐5p with E2F2 and MATN1‐AS1. (Q) Dual‐luciferase reporter assay results of MATN1‐AS1 and E2F2 (Mean ± SEM, Student's t ‐test, ns, no significance, ** p < 0.01, *** p < 0.001). (R) E2F2 expression level changes after being treated with miR‐214‐5p mimics.

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1) Product Images from "MATN1‐AS1 Promotes Tumour Metastasis and Sunitinib Resistance via E2F2 in Clear Cell Renal Cell Carcinoma"

Article Title: MATN1‐AS1 Promotes Tumour Metastasis and Sunitinib Resistance via E2F2 in Clear Cell Renal Cell Carcinoma

Journal: Journal of Cellular and Molecular Medicine

doi: 10.1111/jcmm.70428

MATN1‐AS1 regulates E2F2 expression in ccRCC. (A) Heatmap showing DEGs expression profiles of 786‐O cells transfected with control (Control 1–3) or MATN1‐AS1 targeted sequence (sh 1–3). Data were normalised with FPKM. Results were filtered with p < 0.05, |log 2 FC| > 1. (B, C) GSEA of Control and MATN1‐AS1 knocked down groups. (D) Heatmap showing the expression level changes of the E2F family after knocking down MATN1‐AS1. Data were normalised with FPKM. (E) Co‐expression analysis of E2Fs with MATN1‐AS1 in TCGA‐KIRC dataset (Pearson correlation test). (F) Expression correlation between E2F2 and MATN1‐AS1 in TCGA‐KIRC dataset (Pearson correlation test). (G) E2F2 expression levels in ccRCC and normal tissues in the TCGA‐KIRC dataset (Data were normalised with log 2 (TPM + 1), Mean ± SEM, Wilcoxon test, *** p < 0.001). (H) E2F2 expression levels in ccRCC and normal tissues in the ICGC‐RECA dataset (Data were normalised with log 2 (TPM + 1), Mean ± SEM, Wilcoxon test, *** p < 0.001). (I) Overall survival (OS) curves of E2F2 in ccRCC (Log‐rank test, * p < 0.05). (J, K) GSEA between High‐ and Low‐E2F2 expression individuals from TCGA‐KIRC dataset. (L) E2F2 expression level changes after knocking down MATN1‐AS1. (M) Potential micro‐RNA links between MATN1‐AS1 and E2F2. (N) miR‐214‐5p expression levels in ccRCC and renal tissue from TCGA‐KIRC dataset ( p = 2.2 × 10 −13 ). (O, P) Binding sites schematic diagrams of miR‐214‐5p with E2F2 and MATN1‐AS1. (Q) Dual‐luciferase reporter assay results of MATN1‐AS1 and E2F2 (Mean ± SEM, Student's t ‐test, ns, no significance, ** p < 0.01, *** p < 0.001). (R) E2F2 expression level changes after being treated with miR‐214‐5p mimics.

Figure Legend Snippet: MATN1‐AS1 regulates E2F2 expression in ccRCC. (A) Heatmap showing DEGs expression profiles of 786‐O cells transfected with control (Control 1–3) or MATN1‐AS1 targeted sequence (sh 1–3). Data were normalised with FPKM. Results were filtered with p < 0.05, |log 2 FC| > 1. (B, C) GSEA of Control and MATN1‐AS1 knocked down groups. (D) Heatmap showing the expression level changes of the E2F family after knocking down MATN1‐AS1. Data were normalised with FPKM. (E) Co‐expression analysis of E2Fs with MATN1‐AS1 in TCGA‐KIRC dataset (Pearson correlation test). (F) Expression correlation between E2F2 and MATN1‐AS1 in TCGA‐KIRC dataset (Pearson correlation test). (G) E2F2 expression levels in ccRCC and normal tissues in the TCGA‐KIRC dataset (Data were normalised with log 2 (TPM + 1), Mean ± SEM, Wilcoxon test, *** p < 0.001). (H) E2F2 expression levels in ccRCC and normal tissues in the ICGC‐RECA dataset (Data were normalised with log 2 (TPM + 1), Mean ± SEM, Wilcoxon test, *** p < 0.001). (I) Overall survival (OS) curves of E2F2 in ccRCC (Log‐rank test, * p < 0.05). (J, K) GSEA between High‐ and Low‐E2F2 expression individuals from TCGA‐KIRC dataset. (L) E2F2 expression level changes after knocking down MATN1‐AS1. (M) Potential micro‐RNA links between MATN1‐AS1 and E2F2. (N) miR‐214‐5p expression levels in ccRCC and renal tissue from TCGA‐KIRC dataset ( p = 2.2 × 10 −13 ). (O, P) Binding sites schematic diagrams of miR‐214‐5p with E2F2 and MATN1‐AS1. (Q) Dual‐luciferase reporter assay results of MATN1‐AS1 and E2F2 (Mean ± SEM, Student's t ‐test, ns, no significance, ** p < 0.01, *** p < 0.001). (R) E2F2 expression level changes after being treated with miR‐214‐5p mimics.

Techniques Used: Expressing, Transfection, Control, Sequencing, Binding Assay, Luciferase, Reporter Assay

MATN1‐AS1/miR‐214‐5p/E2F2 axis regulated EMT in ccRCC. (A, B) Cell viability of indicated groups measured with CCK8 assay (Mean ± SEM, Two‐way repeated‐measures analysis of ANOVA with Geisser–Greenhouse correction, ns, no significance, ** p < 0.01, *** p < 0.001). (C) Cell migration and invasion abilities of corresponding groups as measured with the Transwell assay. (D, E) RNA expression level changes of E2F2 after overexpression miR‐214‐5p in 786‐O and A‐498 cell lines. (F, G) RNA expression levels of E2F2 and MATN1‐AS1 in indicated cells. (H, I) E2F2 and EMT biomarkers expression changes across four groups.

Figure Legend Snippet: MATN1‐AS1/miR‐214‐5p/E2F2 axis regulated EMT in ccRCC. (A, B) Cell viability of indicated groups measured with CCK8 assay (Mean ± SEM, Two‐way repeated‐measures analysis of ANOVA with Geisser–Greenhouse correction, ns, no significance, ** p < 0.01, *** p < 0.001). (C) Cell migration and invasion abilities of corresponding groups as measured with the Transwell assay. (D, E) RNA expression level changes of E2F2 after overexpression miR‐214‐5p in 786‐O and A‐498 cell lines. (F, G) RNA expression levels of E2F2 and MATN1‐AS1 in indicated cells. (H, I) E2F2 and EMT biomarkers expression changes across four groups.

Techniques Used: CCK-8 Assay, Migration, Transwell Assay, RNA Expression, Over Expression, Expressing

MATN1‐AS1/miR‐214‐5p/E2F2 axis affects tumour metastasis in ccRCC. (A) Four groups of nude mice were subcutaneously injected with response cells, and tumours were removed and imaged. (B) Tumour volumes were measured every 3 days and drawn as a curve plot (Mean ± SEM, Two‐way repeated‐measures ANOVA with Dunnett multiple comparisons test correction, ns, no significance, *** p < 0.001). (C, D) Four groups of nude mice were tail vein‐injected corresponsive cells and imaged after 6 months (Signals were normalised as p/s/cm2/sr, Mean ± SEM, Student's t ‐test, ns, no significance, * p < 0.05). (E) E2F2, N‐cadherin, and E‐cadherin expression levels in four groups of subcutaneously generated tumours as detected by IHC using serial slices.

Figure Legend Snippet: MATN1‐AS1/miR‐214‐5p/E2F2 axis affects tumour metastasis in ccRCC. (A) Four groups of nude mice were subcutaneously injected with response cells, and tumours were removed and imaged. (B) Tumour volumes were measured every 3 days and drawn as a curve plot (Mean ± SEM, Two‐way repeated‐measures ANOVA with Dunnett multiple comparisons test correction, ns, no significance, *** p < 0.001). (C, D) Four groups of nude mice were tail vein‐injected corresponsive cells and imaged after 6 months (Signals were normalised as p/s/cm2/sr, Mean ± SEM, Student's t ‐test, ns, no significance, * p < 0.05). (E) E2F2, N‐cadherin, and E‐cadherin expression levels in four groups of subcutaneously generated tumours as detected by IHC using serial slices.

Techniques Used: Injection, Expressing, Generated

Knocking down MATN1‐AS1 reversed drug resistance in sunitinib resistance ccRCC. (A, B) GSEA of drug resistance signalling pathway. (C) DEGs between sunitinib resistance ccRCC cells and non‐treated cells of the GSE216494 dataset (|FDR| < 1, p < 0.05 was defined as non‐significance expressed genes filter criteria). (D) MATN1‐AS1 expression levels between sunitinib resistance ccRCC cells and non‐treated cells. (E) Gene ontology analysis of DEGs between sunitinib resistance ccRCC cells and non‐treated cells. (F) Graph diagram of sunitinib resistance A‐498 cell line (A‐498‐R) establishing process. (G) IC50 curves of sunitinib in A‐498 and A‐498‐R cell lines. (Data were presented as mean ± SEM). (H, I) MATN1‐AS1 and E2F2 RNA expression values between A‐498 and A‐498‐R cell lines (Mean ± SEM, Student's t ‐test, ** p < 0.01, *** p < 0.001). (J) E2F2 expression levels of A‐498 and A‐498‐R cells. (K) Knocking down MATN1‐AS1 inhibited cell viability of the A‐498‐R cell line cultured in 10 μM sunitinib (Mean ± SEM, Two‐way ANOVA, *** p < 0.001). (L) Drug‐response curves of sunitinib in MATN1‐AS1 knocked down A‐498‐R cells and non‐treated A‐498‐R cells (Mean ± SEM, Two‐way ANOVA test, *** p < 0.001). (M) Overexpression E2F2 reversed cell viability of the A‐498‐R cell line treated with 10 μM sunitinib (Mean ± SEM, Two‐way ANOVA, ** p < 0.01). (N) Drug‐response curves of sunitinib in E2F2 overexpressed A‐498‐R cells and non‐treated A‐498‐R cells (Mean ± SEM, Two‐way ANOVA test, *** p < 0.001). (O) Drug‐response curves of sunitinib in indicated groups (Mean ± SEM, Two‐way ANOVA test, ns, no significance, *** p < 0.001).

Figure Legend Snippet: Knocking down MATN1‐AS1 reversed drug resistance in sunitinib resistance ccRCC. (A, B) GSEA of drug resistance signalling pathway. (C) DEGs between sunitinib resistance ccRCC cells and non‐treated cells of the GSE216494 dataset (|FDR| < 1, p < 0.05 was defined as non‐significance expressed genes filter criteria). (D) MATN1‐AS1 expression levels between sunitinib resistance ccRCC cells and non‐treated cells. (E) Gene ontology analysis of DEGs between sunitinib resistance ccRCC cells and non‐treated cells. (F) Graph diagram of sunitinib resistance A‐498 cell line (A‐498‐R) establishing process. (G) IC50 curves of sunitinib in A‐498 and A‐498‐R cell lines. (Data were presented as mean ± SEM). (H, I) MATN1‐AS1 and E2F2 RNA expression values between A‐498 and A‐498‐R cell lines (Mean ± SEM, Student's t ‐test, ** p < 0.01, *** p < 0.001). (J) E2F2 expression levels of A‐498 and A‐498‐R cells. (K) Knocking down MATN1‐AS1 inhibited cell viability of the A‐498‐R cell line cultured in 10 μM sunitinib (Mean ± SEM, Two‐way ANOVA, *** p < 0.001). (L) Drug‐response curves of sunitinib in MATN1‐AS1 knocked down A‐498‐R cells and non‐treated A‐498‐R cells (Mean ± SEM, Two‐way ANOVA test, *** p < 0.001). (M) Overexpression E2F2 reversed cell viability of the A‐498‐R cell line treated with 10 μM sunitinib (Mean ± SEM, Two‐way ANOVA, ** p < 0.01). (N) Drug‐response curves of sunitinib in E2F2 overexpressed A‐498‐R cells and non‐treated A‐498‐R cells (Mean ± SEM, Two‐way ANOVA test, *** p < 0.001). (O) Drug‐response curves of sunitinib in indicated groups (Mean ± SEM, Two‐way ANOVA test, ns, no significance, *** p < 0.001).

Techniques Used: Expressing, RNA Expression, Cell Culture, Over Expression

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Journal: Journal of Cellular and Molecular Medicine

Article Title: MATN1‐AS1 Promotes Tumour Metastasis and Sunitinib Resistance via E2F2 in Clear Cell Renal Cell Carcinoma

doi: 10.1111/jcmm.70428

Figure Lengend Snippet: MATN1‐AS1 regulates E2F2 expression in ccRCC. (A) Heatmap showing DEGs expression profiles of 786‐O cells transfected with control (Control 1–3) or MATN1‐AS1 targeted sequence (sh 1–3). Data were normalised with FPKM. Results were filtered with p < 0.05, |log 2 FC| > 1. (B, C) GSEA of Control and MATN1‐AS1 knocked down groups. (D) Heatmap showing the expression level changes of the E2F family after knocking down MATN1‐AS1. Data were normalised with FPKM. (E) Co‐expression analysis of E2Fs with MATN1‐AS1 in TCGA‐KIRC dataset (Pearson correlation test). (F) Expression correlation between E2F2 and MATN1‐AS1 in TCGA‐KIRC dataset (Pearson correlation test). (G) E2F2 expression levels in ccRCC and normal tissues in the TCGA‐KIRC dataset (Data were normalised with log 2 (TPM + 1), Mean ± SEM, Wilcoxon test, *** p < 0.001). (H) E2F2 expression levels in ccRCC and normal tissues in the ICGC‐RECA dataset (Data were normalised with log 2 (TPM + 1), Mean ± SEM, Wilcoxon test, *** p < 0.001). (I) Overall survival (OS) curves of E2F2 in ccRCC (Log‐rank test, * p < 0.05). (J, K) GSEA between High‐ and Low‐E2F2 expression individuals from TCGA‐KIRC dataset. (L) E2F2 expression level changes after knocking down MATN1‐AS1. (M) Potential micro‐RNA links between MATN1‐AS1 and E2F2. (N) miR‐214‐5p expression levels in ccRCC and renal tissue from TCGA‐KIRC dataset ( p = 2.2 × 10 −13 ). (O, P) Binding sites schematic diagrams of miR‐214‐5p with E2F2 and MATN1‐AS1. (Q) Dual‐luciferase reporter assay results of MATN1‐AS1 and E2F2 (Mean ± SEM, Student's t ‐test, ns, no significance, ** p < 0.01, *** p < 0.001). (R) E2F2 expression level changes after being treated with miR‐214‐5p mimics.

Article Snippet: Antibody reagents were anti‐E2F2 (1:1000; bsm‐52641R; Bioss), anti‐SNAI1 (1:1000; 13099‐1‐AP; Proteintech), anti‐SNAI2 (1:1000; 12129‐1‐AP; Proteintech), anti‐Vimentin (1:1000; 10366‐1‐AP; Proteintech), anti‐N‐cadherin (1:1000; 22018‐1‐AP; Proteintech), anti‐E‐cadherin (1:1000; no. 3195; CST), and anti‐GAPDH (1:2000; no. 2118; CST).

Techniques: Expressing, Transfection, Control, Sequencing, Binding Assay, Luciferase, Reporter Assay

Journal: Journal of Cellular and Molecular Medicine

Article Title: MATN1‐AS1 Promotes Tumour Metastasis and Sunitinib Resistance via E2F2 in Clear Cell Renal Cell Carcinoma

doi: 10.1111/jcmm.70428

Figure Lengend Snippet: MATN1‐AS1/miR‐214‐5p/E2F2 axis regulated EMT in ccRCC. (A, B) Cell viability of indicated groups measured with CCK8 assay (Mean ± SEM, Two‐way repeated‐measures analysis of ANOVA with Geisser–Greenhouse correction, ns, no significance, ** p < 0.01, *** p < 0.001). (C) Cell migration and invasion abilities of corresponding groups as measured with the Transwell assay. (D, E) RNA expression level changes of E2F2 after overexpression miR‐214‐5p in 786‐O and A‐498 cell lines. (F, G) RNA expression levels of E2F2 and MATN1‐AS1 in indicated cells. (H, I) E2F2 and EMT biomarkers expression changes across four groups.

Techniques: CCK-8 Assay, Migration, Transwell Assay, RNA Expression, Over Expression, Expressing

Journal: Journal of Cellular and Molecular Medicine

Article Title: MATN1‐AS1 Promotes Tumour Metastasis and Sunitinib Resistance via E2F2 in Clear Cell Renal Cell Carcinoma

doi: 10.1111/jcmm.70428

Figure Lengend Snippet: MATN1‐AS1/miR‐214‐5p/E2F2 axis affects tumour metastasis in ccRCC. (A) Four groups of nude mice were subcutaneously injected with response cells, and tumours were removed and imaged. (B) Tumour volumes were measured every 3 days and drawn as a curve plot (Mean ± SEM, Two‐way repeated‐measures ANOVA with Dunnett multiple comparisons test correction, ns, no significance, *** p < 0.001). (C, D) Four groups of nude mice were tail vein‐injected corresponsive cells and imaged after 6 months (Signals were normalised as p/s/cm2/sr, Mean ± SEM, Student's t ‐test, ns, no significance, * p < 0.05). (E) E2F2, N‐cadherin, and E‐cadherin expression levels in four groups of subcutaneously generated tumours as detected by IHC using serial slices.

Techniques: Injection, Expressing, Generated

Journal: Journal of Cellular and Molecular Medicine

Article Title: MATN1‐AS1 Promotes Tumour Metastasis and Sunitinib Resistance via E2F2 in Clear Cell Renal Cell Carcinoma

doi: 10.1111/jcmm.70428

Figure Lengend Snippet: Knocking down MATN1‐AS1 reversed drug resistance in sunitinib resistance ccRCC. (A, B) GSEA of drug resistance signalling pathway. (C) DEGs between sunitinib resistance ccRCC cells and non‐treated cells of the GSE216494 dataset (|FDR| < 1, p < 0.05 was defined as non‐significance expressed genes filter criteria). (D) MATN1‐AS1 expression levels between sunitinib resistance ccRCC cells and non‐treated cells. (E) Gene ontology analysis of DEGs between sunitinib resistance ccRCC cells and non‐treated cells. (F) Graph diagram of sunitinib resistance A‐498 cell line (A‐498‐R) establishing process. (G) IC50 curves of sunitinib in A‐498 and A‐498‐R cell lines. (Data were presented as mean ± SEM). (H, I) MATN1‐AS1 and E2F2 RNA expression values between A‐498 and A‐498‐R cell lines (Mean ± SEM, Student's t ‐test, ** p < 0.01, *** p < 0.001). (J) E2F2 expression levels of A‐498 and A‐498‐R cells. (K) Knocking down MATN1‐AS1 inhibited cell viability of the A‐498‐R cell line cultured in 10 μM sunitinib (Mean ± SEM, Two‐way ANOVA, *** p < 0.001). (L) Drug‐response curves of sunitinib in MATN1‐AS1 knocked down A‐498‐R cells and non‐treated A‐498‐R cells (Mean ± SEM, Two‐way ANOVA test, *** p < 0.001). (M) Overexpression E2F2 reversed cell viability of the A‐498‐R cell line treated with 10 μM sunitinib (Mean ± SEM, Two‐way ANOVA, ** p < 0.01). (N) Drug‐response curves of sunitinib in E2F2 overexpressed A‐498‐R cells and non‐treated A‐498‐R cells (Mean ± SEM, Two‐way ANOVA test, *** p < 0.001). (O) Drug‐response curves of sunitinib in indicated groups (Mean ± SEM, Two‐way ANOVA test, ns, no significance, *** p < 0.001).

Techniques: Expressing, RNA Expression, Cell Culture, Over Expression

Correlation between experimental and clinical expression of niclosamide-regulated genes. ( A ) BRIP1, E2F2, FANCA, DNA2, and TTK mRNA expression levels in normal tissue (NT) and primary tumor tissue (TP) from TCGA-KIRC dataset. ( B ) A-498 and ACHN cells were treated with 2.5 µM sunitinib, 1 µM niclosamide, or their combination, for 48 h. Protein expression of BRIP, E2F2, and FANCA was detected by Western blot; GAPDH was a loading control. Representative blots from n = 3 independent experiments are shown. Densitometric quantification of γ-H2AX relative to GAPDH is presented as mean ± SD (n = 3). Statistical significance was determined by one-way ANOVA with post hoc tests. (* p < 0.05 compared to control). D, DMSO; S, sunitinib; N, niclosamide; C, combination.

Journal: International Journal of Molecular Sciences

Article Title: Novel Therapeutic Strategy for Renal Cell Carcinoma: Niclosamide Enhances Sunitinib Efficacy via DNA Repair and Cell Cycle Pathways

doi: 10.3390/ijms262210922

Figure Lengend Snippet: Correlation between experimental and clinical expression of niclosamide-regulated genes. ( A ) BRIP1, E2F2, FANCA, DNA2, and TTK mRNA expression levels in normal tissue (NT) and primary tumor tissue (TP) from TCGA-KIRC dataset. ( B ) A-498 and ACHN cells were treated with 2.5 µM sunitinib, 1 µM niclosamide, or their combination, for 48 h. Protein expression of BRIP, E2F2, and FANCA was detected by Western blot; GAPDH was a loading control. Representative blots from n = 3 independent experiments are shown. Densitometric quantification of γ-H2AX relative to GAPDH is presented as mean ± SD (n = 3). Statistical significance was determined by one-way ANOVA with post hoc tests. (* p < 0.05 compared to control). D, DMSO; S, sunitinib; N, niclosamide; C, combination.

Article Snippet: The membranes were blocked and subsequently incubated overnight at 4 °C with specific primary antibodies against BRIP1 (Cell Signaling Technology), E2F2 (Santa Cruz Biotechnology, Inc., Dallas, TX, USA), FANCA (Cell Signaling Technology), γH2AX (Ser139; Cell Signaling Technology), Cyclin A (Santa Cruz Biotechnology, Inc.), Cyclin B (Santa Cruz Biotechnology, Inc.), CDK1 (Santa Cruz Biotechnology, Inc.), β-actin (Santa Cruz Biotechnology, Inc.), and GAPDH (Santa Cruz Biotechnology, Inc.).

Techniques: Expressing, Western Blot, Control

a Immunoblotting of FTO in FTO knockdown RWPE1 and control RWPE1 cells is presented. b The distribution of peaks is shown with a significant change in m 6 A level in FTO knockdown RWPE1 cells compared to control RWPE1 cells. c A Venn diagram shows the shared genes between increased m 6 A peaks upon FTO deletion and FTO-relation genes analyzed by RNA-seq. A total of 236 genes were observed. d , e Pathway analysis and KEGG analysis of the above 236 shared genes showed that the cell cycle was altered in FTO knockdown cells. f The mapped reads represent enriched RNA fragments by MeRIP-seq. RNA methylation profiles were loaded in IGV software and m 6 A modification peak alterations in CDKN2C and E2F2 mRNA full length were visualized. g MeRIP-qRT-PCR was used to detect the m 6 A levels alterations of CDKN2C and E2F2 after knocking down FTO in RWPE1 cells. h Cell cycle distribution of FTO silencing cells and control cells was analyzed by flow cytometry. i E2F2 and CDKN2C were detected by western blot in ZFHX3 knockdown cells or control cells where FTO was silenced with siRNA targeting FTO or siCtrl. ** P < 0.01; *** P < 0.001, ns not significant.

Journal: Cell Death Discovery

Article Title: ZFHX3 acts as a tumor suppressor in prostate cancer by targeting FTO-mediated m 6 A demethylation

doi: 10.1038/s41420-024-02060-w

Figure Lengend Snippet: a Immunoblotting of FTO in FTO knockdown RWPE1 and control RWPE1 cells is presented. b The distribution of peaks is shown with a significant change in m 6 A level in FTO knockdown RWPE1 cells compared to control RWPE1 cells. c A Venn diagram shows the shared genes between increased m 6 A peaks upon FTO deletion and FTO-relation genes analyzed by RNA-seq. A total of 236 genes were observed. d , e Pathway analysis and KEGG analysis of the above 236 shared genes showed that the cell cycle was altered in FTO knockdown cells. f The mapped reads represent enriched RNA fragments by MeRIP-seq. RNA methylation profiles were loaded in IGV software and m 6 A modification peak alterations in CDKN2C and E2F2 mRNA full length were visualized. g MeRIP-qRT-PCR was used to detect the m 6 A levels alterations of CDKN2C and E2F2 after knocking down FTO in RWPE1 cells. h Cell cycle distribution of FTO silencing cells and control cells was analyzed by flow cytometry. i E2F2 and CDKN2C were detected by western blot in ZFHX3 knockdown cells or control cells where FTO was silenced with siRNA targeting FTO or siCtrl. ** P < 0.01; *** P < 0.001, ns not significant.

Article Snippet: The primary antibodies used in western blot were as follows: anti-ACTIN (20536-1-AP, Proteintech), anti-ZFHX3 (PD010, MBL), anti-FTO (27226-1-AP, Proteintech), anti-MYC (TA150121, OriGene), anti-E2F2 (ab138515, Abcam), and anti-CDKN2C (ab192239, Abcam).

Techniques: Western Blot, RNA Sequencing Assay, Methylation, Software, Modification, Quantitative RT-PCR, Flow Cytometry

ZFHX3 suppressed the transcription of FTO , which increased the m 6 A modification of target genes, including ZFHX3 , E2F2 , and CDKN2C . Meanwhile, ZFHX3 was regulated by FTO through m 6 A modification.

Journal: Cell Death Discovery

Article Title: ZFHX3 acts as a tumor suppressor in prostate cancer by targeting FTO-mediated m 6 A demethylation

doi: 10.1038/s41420-024-02060-w

Figure Lengend Snippet: ZFHX3 suppressed the transcription of FTO , which increased the m 6 A modification of target genes, including ZFHX3 , E2F2 , and CDKN2C . Meanwhile, ZFHX3 was regulated by FTO through m 6 A modification.

Techniques: Modification

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