Journal: Current Oncology

Article Title: E2F1-Driven WDHD1 Transcription Enhances Cell-Cycle Progression and Promotes Pancreatic Cancer Progression

doi: 10.3390/curroncol33040186

Figure Lengend Snippet: The E2F1–WDHD1 axis promotes malignant phenotypes in pancreatic cancer by upregulating cyclin D1. ( A , B ) Expression of cell cycle-related proteins after knocking down WDHD1. β-actin served as a loading control; Representative images were selected from three independent experiments. ( C ) Expression of CDK4 and cyclin D proteins after overexpression of WDHD1. β-actin served as a loading control. Representative images were selected from three independent experiments. ( D ) RNA expression levels of E2F1 in various pancreatic cancer cell lines show elevated expression compared to normal pancreatic cell lines ( n = 3 independent biological replicates). Summary statistics for each experimental group reported as means ± SD. Statistical significance: * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 (Student’s t -test), ns, non-significant. ( E , F ) Overexpression of E2F1 can increase the expression of WDHD1 at both the RNA and protein levels ( n = 4 independent biological replicates). Summary statistics for each experimental group reported as means ± SD. Statistical significance: * p < 0.05, *** p < 0.001 (Student’s t -test). β-actin served as a loading control. Representative images were selected from three independent experiments. ( G ) The impact of WDHD1 knockdown after overexpression of E2F1 on cyclin D1, cyclin D3, and CDK4 at protein level. β-actin served as a loading control. Representative images were selected from three independent experiments. ( H ) E2F1 activates the WDHD1 promoter. E2F1 overexpression significantly increased the activity of a luciferase reporter driven by the full-length WDHD1 promoter relative to the vector control, consistent with direct transcriptional activation of WDHD1 by E2F1 ( n = 3 independent biological replicates). Summary statistics for each experimental group reported as means ± SD; Statistical significance: *** p < 0.001 (Student’s t -test). ( I ) ChIP–qPCR shows enrichment of the WDHD1 promoter in anti-E2F1 immunoprecipitates relative to IgG control ( n = 3 independent biological replicates). Summary statistics for each experimental group reported as means ± SD; Statistical significance: **** p < 0.0001 (Student’s t -test). The unedited blots can be found in .

Article Snippet: The antibodies utilized in this study included anti-WDHD1 (abclonal, A15396, 1:1000), anti-E2F1 (abclonal, A19579, 1:1000), anti-CDK4 (abclonal, A0366, 1:1000), anti-CDK6 (abclonal, A1545, 1:1000), anti-cyclin D1 (abclonal, A1301, 1:1000), and anti-cyclin D3 (abclonal, A3589, 1:1000). β-actin (ZSGB-BIO, TA-09, 1:1000) was used as the sample loading control.

Techniques: Expressing, Control, Over Expression, RNA Expression, Knockdown, Activity Assay, Luciferase, Plasmid Preparation, Activation Assay, ChIP-qPCR

Journal: bioRxiv

Article Title: “Targeting LARP1 Enhances Carboplatin Sensitivity and Suppresses Tumor Growth in Endometrial Cancer”

doi: 10.64898/2026.03.22.713473

Figure Lengend Snippet: (A, B) Kaplan–Meier plot showing that overexpression of E2F1 is associated with shorter overall survival (A) and progression-free interval (B) in endometrial cancer cohort. (C, D) Kaplan–Meier plot showing that co-overexpression of LARP1 and E2F1 is associated with shorter overall survival (C) and progression-free interval (D) in endometrial cancer cohort. (E) Spearman correlation analysis shows a correlation between LARP1 and E2F1 in endometrial cancer patients.

Article Snippet: Cells were then incubated overnight at 4 °C with the following primary antibodies: LARP1 (Cat. No. sc-515873; 1:200 dilution; Santa Cruz Biotechnology, Dallas, TX, USA) and E2F1 (Cat. No. 3742S; 1:400 dilution; Cell Signaling Technology, Danvers, MA, USA).

Techniques: Over Expression

Journal: bioRxiv

Article Title: “Targeting LARP1 Enhances Carboplatin Sensitivity and Suppresses Tumor Growth in Endometrial Cancer”

doi: 10.64898/2026.03.22.713473

Figure Lengend Snippet: (A, B) Immunoblot analysis showing the protein expression of LARP1 and E2F1 after transfecting ISHI (A) and HEC-1A (B) cells with control or LARP1 siRNA. β-actin was used as a loading control. (C) Images representing immunofluorescence staining of LARP1 (green) and E2F1 (red) in HEC-1A cells after transfection with control or LARP1 siRNA. DAPI was used as a counter stain. Scale bar = 50 µm.

Article Snippet: Cells were then incubated overnight at 4 °C with the following primary antibodies: LARP1 (Cat. No. sc-515873; 1:200 dilution; Santa Cruz Biotechnology, Dallas, TX, USA) and E2F1 (Cat. No. 3742S; 1:400 dilution; Cell Signaling Technology, Danvers, MA, USA).

Techniques: Western Blot, Expressing, Control, Immunofluorescence, Staining, Transfection

Journal: Frontiers in Pharmacology

Article Title: Effect of the antifungal drug ciclopirox on the inhibition of HMGA2-mediated oncogenic capacity in ACHN renal cell carcinoma

doi: 10.3389/fphar.2026.1723954

Figure Lengend Snippet: Effect of CPX on the expression of E-cadherin, N-cadherin, TGF-β R II, Smad-2, Smad-3, and Snail in tumor tissues. (A) Expression levels of E-cadherin, N-cadherin, TGF-β R II, Smad-2, Smad-3, and Snail in tumor tissues detected by qRT-PCR. (B) The expression levels of HMGA2, E2F1, Cyclin D1 and CDK6 in tumor tissues were examined by protein blotting (C) . Quantitation of the result of Western blot. Values are shown as mean ± SD. * P < 0.05 vs. control group, * ** P < 0.001 vs. control group.

Article Snippet: Antibodies against HMGA2 (ER62068), E2F1 (ET1701-73), CyclinD1 (ET1601-31), E-cadherin (ET1607-75), N-cadherin (ET1607-37), Smad2 (ET1604-22), Smad3 (ET1607-41), TGFR II (ER 1917-66), and Snai1 (ER1706-22) were purchased from HuaBio (Hangzhou, China), and CDK6 (ab124821) antibody was purchased from Abcam (Cambridge, United Kingdom).

Techniques: Expressing, Quantitative RT-PCR, Quantitation Assay, Western Blot, Control

Journal: Frontiers in Pharmacology

Article Title: Effect of the antifungal drug ciclopirox on the inhibition of HMGA2-mediated oncogenic capacity in ACHN renal cell carcinoma

doi: 10.3389/fphar.2026.1723954

Figure Lengend Snippet: Effect of CPX on the expression of HMGA2,E2F1, Cyclin D1, and CDK6 in renal cancer ACHN cells. (A) Expression levels of HMGA2,E2F1, Cyclin D1 and CDK6 in tumor tissues detected by qRT-PCR. (B) The expression levels of HMGA2, E2F1, Cyclin D1, and CDK6 in renal cancer ACHN cells examined by protein blotting. (C) Quantitation of the result of Western blot. Values are shown as mean ± SD. * P < 0.05 vs. control group, * ** P < 0.001 vs. control group. (D) The expression levels of HMGA2, E2F1, Cyclin D1, and CDK6 in renal cancer ACHN cells examined by qRT-PCR. (E) Quantitation of the result of Western blot.

Article Snippet: Antibodies against HMGA2 (ER62068), E2F1 (ET1701-73), CyclinD1 (ET1601-31), E-cadherin (ET1607-75), N-cadherin (ET1607-37), Smad2 (ET1604-22), Smad3 (ET1607-41), TGFR II (ER 1917-66), and Snai1 (ER1706-22) were purchased from HuaBio (Hangzhou, China), and CDK6 (ab124821) antibody was purchased from Abcam (Cambridge, United Kingdom).

Techniques: Expressing, Quantitative RT-PCR, Quantitation Assay, Western Blot, Control