E2F5 (E2F Transcription Factor 5)

And the binding potential between those components in FZXYSJD and E2F5 was confirmed through molecular docking. FZXYSJD affects cell proliferation in RCC through the E2F5 gene.

Integration of transcriptomics and spatial validation revealed robust CD36-mediated immunometabolic signaling in AML, which further requires comprehensive in-vitro and in-vivo validation.

E2F5 is highly expressed in LSCC and is associated with the regulation of NETs-related genes. It may contribute to tumor proliferation and immune evasion by reshaping the tumor microenvironment, highlighting E2F5 as a potential therapeutic target that warrants further functional validation.

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.

This study established a prognostic model of HCC based on cellular senescence-related gene expression. Our findings may provide insights that can be used to develop novel potential targeted therapies.

BPH tissues served as control samples. EVs from blood plasma might serve as a potential liquid biopsy marker for predicting disease progression and better prognosis.

In vivo, SH514 effectively inhibited the proliferation of MM tumors, showing much better antitumor efficacy than the clinical drug lenalidomide, and exhibited no significant toxicity. Thus, these IRF4 inhibitors could serve as promising leads for the development of novel anti-multiple myeloma agents.

The E2F transcription factor family induces prostate cancer and correlates with poor prognosis. E2F1 directly regulates TMEM132A by binding its promoter and controlling the degree of protein expression, thereby affecting cancer cell growth.

Based on these findings, we propose that loss of E2F5 leads to altered regulation of Cyclin D1, which facilitates the development of metastatic mammary tumors after long latency. More importantly, this study demonstrates that conditional loss of E2F5 in the mammary gland leads to tumor formation, revealing its role as a transcription factor regulating a network of genes that normally result in a tumor suppressor function.

Also, knockdown of IMP3 inhibited allograft tumor progression in vivo. These studies reveal the molecular mechanism by which IMP3 regulates E2F5 mRNA stability and identify IMP3/E2F5 as a potential therapeutic target in OSCC.

E2F5 targeted by let-7d-5p facilitated cell proliferation, metastasis and immune escape in GBC through the JAK2/STAT3 pathway.

In conclusion, LINC01980, activated by the canonical TGF-β/SMAD pathway, promoted HCC metastasis via miR-376b-5p/E2F5 axis. Therefore, LINC01980 might be a potential prognostic biomarker and therapeutic target of HCC.