E2F2 (E2F Transcription Factor 2)

Functional assays confirm that ononin-induced repression of E2F2 impairs DNA repair capacity and increases cisplatin sensitivity in cisplatin-resistant PTC cells. These findings identify ononin as a promising adjuvant candidate for overcoming cisplatin resistance in PTC by targeting the E2F2/MDC1-dependent DDR pathway.

The identification and validation of biomarkers reflecting this continuum could enable the establishment of molecular margins-improving risk assessment, reducing local recurrence, and advancing personalized oncologic surgery in HNSCC. Standardizing definitions and sampling protocols for "normal adjacent tissue" remains essential for future translational research.

Functional studies established that E2F2 directly regulates FZD10 expression, activating the Wnt/β-catenin pathway to sustain the stem-like state. Collectively, we unveil the E2F2/FZD10 axis as a previously unrecognized molecular conduit through which environmental arsenic reprograms mammary epithelial cells toward a BCSCs-like phenotype, providing mechanistic insight into arsenic-associated breast cancer risk and revealing a potential target for preventive intervention.

Our study identifies HMGB1 as a key oncogenic driver in NF1-MPNST progression, functioning through direct transcriptional activation of E2F2 to promote cell cycle progression and tumor malignancy. These findings position HMGB1 as both a prognostic biomarker and a promising therapeutic target for NF1-associated MPNSTs.

Collectively, our study establishes miR-31 as a novel biomarker for LUAD proliferative potential and implicates the miR-31/CDK1-E2F2 network as a promising target for disrupting LUAD progression. These findings establish a miRNA-centric precision therapeutic paradigm for effectively suppressing oncogenic proliferation in LUAD.

Since loss of the tumor suppressor APC is common in TNBC, we investigated how APC depletion alters transcriptional adaptation to chemotherapy using RNA-seq profiling of MDA-MB-157 cells and APC knockdown derivatives under control, cisplatin, and paclitaxel treatment. Machine-learning feature selection (Random Forest + PLS-DA) identified a 43-gene discriminant signature enriched for regulators of cell cycle and DNA repair (CCNB3, ORC1, E2F2, UNG), cytokine signaling (CXCL2, IL11), and metabolic support. These findings suggest that APC loss primes TNBC cells for chemotherapy persistence through an energetically reinforced, transcriptionally flexible survival program, highlighting DDR-OXPHOS-translation and inflammatory circuits as potential therapeutic vulnerabilities.

In summary, maternal undernutrition disrupted male fetal rumen metabolism and elevated novel miR-736, which targeted and downregulated E2F2 and MYBL2 to inhibit cell cycle progression and promote apoptosis, finally inhibited male fetal rumen development. This study provides new insights into the epigenetic mechanisms underlying maternal undernutrition-induced male fetal rumen developmental deficits.

There existed a positive correlation between E2F2 expression level and Dasatinib sensitivity, negatively related to drug sensitivity of Nelarabine, XK-469, Cyclophosphamide, etc. Pazopanib, Doxorubicin, and Paclitaxel sensitivity was all positively associated with E2F5 expression. According to these analysis and validation results, E2F genes are relevant to the occurrence and progression of various cancers, which may be biomarkers for tumor diagnostics and prognosis. The discovery of new therapeutic targets can lead to reshaping TME to promote tumor-suppressive metastasis rather than tumor-friendly metastasis.

Tyrosine kinase inhibitors (TKIs), such as sunitinib and sorafenib, are standard treatments for renal cell carcinoma (RCC). RNA sequencing (RNA-seq) and bioinformatic analyses showed that niclosamide modulated critical pathways, including BRIP1- and FANCA-mediated DNA repair and E2F2-regulated cell cycle progression. These findings provide proof-of-concept that niclosamide enhances TKI efficacy through modulation of DNA repair and cell cycle pathways, supporting the rationale for DNA damage response (DDR)-targeted combination strategies in RCC.

Inhibition of ACSL4 with PRGL493 suppressed tumor growth in vitro and in vivo. These findings highlight ACSL4 as a dual regulator of lipid metabolism and cell proliferation and a potential therapeutic target in EC.

C1orf50 is a novel biomarker of poor prognosis in HCC and a key regulator of oncogenic features such as EMT, cell cycle progression, and stemness. This study highlights the therapeutic potential of targeting C1orf50-related networks in aggressive subtypes of liver cancer.

In brief, NR2F6, as a nuclear transcription factor, enhances the transcription of E2F2.The increased expression of E2F2 enhances PARP1 expression, which in turn facilitates TMZ-mediated DNA damage repair, thereby diminishing glioma sensitivity to TMZ.