E2F1 (E2F transcription factor 1)

Of these agents, Telomelysin (OBP-301, Suratadenoturev), a telomerase-specific oncolytic adenovirus, demonstrated clinical safety but limited efficacy in refractory tumors. Given its multifaceted antitumor functions and ability to overcome key barriers in pancreatic cancer, OBP-702 represents a highly promising therapeutic candidate. A first-in-human clinical trial evaluating endoscopic ultrasonography-guided intratumoral injection of OBP-702 is currently in preparation, expected to advance clinical translation of this novel virotherapeutic strategy.

On the other hand, NDGA inhibited CBP/p300, decreased H3K27ac levels, and synergized with the EZH2 inhibitor EPZ6438 against PC3 cells. In conclusion, NDGA is a potential epigenetic antineoplastic agent that downregulates EZH2 and H3K27me3 through the NRP1 and PI3K/AKT/mTOR pathways and exerts a synergistic antitumor effect with H3K27ac and EZH2 inhibitors, suggesting that it could be a valuable therapeutic option for prostate cancer.

The study bridges computational predictions with functional evidence, proposing CCDC78 as a novel oncogenic driver in COAD through cell cycle dysregulation. Future investigations will employ in vivo models to delineate its molecular mechanisms.

Collectively, our findings suggested that the downregulation of RB1 significantly influences the morphology of LUAD by facilitating EMT and nuclear abnormalities through HDAC1-mediated deacetylation of lamin A/C. Future research should prioritize the development of targeted therapies aimed at restoring RB1 function or inhibiting HDAC1 to mitigate cancer progression, thereby enhancing patient stratification and treatment strategies in TKI-resistant LUAD.

This study elucidates the critical role and molecular mechanism through which KLF11 drives radiotherapy resistance in ESCC by regulating the MDM2/E2F1 axis and enhancing HR repair, thereby providing a solid theoretical foundation and potential target for the development of KLF11-targeted radiosensitization therapies for ESCC.

Understanding the mechanisms that regulate miRNA transcription in different cancers could help understand the pathology of cancer from a novel perspective with shared TFs constitutive to multiple cancers. This may also open up new avenues for cancer therapeutic innovation, in which miRNA-based interventions might be able to target and be relevant to multiple cancers at once in the future.

Collectively, our findings suggest GlcN as a potential therapeutic agent for HCC and underscore its chemosensitizing potential when combined with lenvatinib. Given GlcN's established clinical safety, this combination offers a translatable strategy for HCC therapy.

Our findings elucidate that the I680T mutation-induced loss-of-function of RB1 simultaneously confers invasive proliferation and chemotherapeutic vulnerability to tumor cells, suggesting that RB1-I680T could serve as a predictive biomarker for chemotherapy response in NSCLC. Stratifying patients based on the RB1-I680T mutation status may enable personalized therapeutic strategies, particularly for tumors with E2F1 dysregulation.

Moreover, E2F1 AS activity was evident as cells progress through the cell cycle and during the DNA damage response, and apparent in tumour models. Our results highlight gene networks where transcription and splicing are linked and coordinated by the pRb-E2F pathway, and further establish the widespread influence that pRb, E2F1, and PRMT5 have on regulating biological diversity through RNA splicing control.

We also demonstrate that knockdown of STAT3 or disruption of STAT3 function in MDA-MB-468 cells opposes the effects of CDK8 inhibition on Mcl-1. Together, these results suggest that CDK8 inhibitor treatment can modulate the expression of apoptosis-related proteins p73 and Mcl-1 and continues to highlight the potential cooperative effects of E2F1 and STAT3 in the activity of CDK8 inhibitor against MDA-MB-468 triple-negative breast cancer cells.

E2F1 promoted CHOL synthesis and PCa tumor growth in vivo. E2F1 enhanced cell proliferation, invasion, and tumor growth by enhancing CHOL synthesis via the SND1/ACLY axis in PCa models.

This study established a telomere-based prognostic model for HCC. This model provides reliable survival prediction, captures key tumor microenvironment features, and yields insights to support personalized therapeutic strategies, offering a valuable tool for clinical decision-making in HCC.