TRIM35 (Tripartite Motif Containing 35)

In conclusion, our study demonstrates that TRIM35 regulates the ubiquitination of EIF3E and inhibits the CDK4/Cyclin D1 signaling pathway, thereby suppressing the malignant proliferation of EC. These findings suggested that TRIM35 has potential as a therapeutic target for EC.

Notably, among the genes regulated, Heat Shock Protein Family A (Hsp70) Member 6 (HSPA6) is significantly upregulated through TRIM35-mediated transcriptional regulation, which suppresses breast cancer progression and mediates TRIM35's anti-tumor effect. Collectively, our findings reveal a previously unrecognized mechanism by which TRIM35 regulates gene expression through targeted epigenetic modification, providing new insights into its tumor-suppressive role in breast cancer.

We found that increased P53 transcriptional activity (in cardiomyocyte-specific Trim35 overexpression transgenic mice) was sufficient to initiate heart failure and these molecular findings were recapitulated in nonischemic human LV dilated cardiomyopathy samples. These findings suggest that TRIM35 and the K120Ub-histone 2B epigenetic modification are molecular features of cardiomyocytes that can collectively predict dilated cardiomyopathy pathogenesis.

These findings reveal that HBO regulates the Warburg effect of hypoxic HCC cells through miR-103a-3p/TRIM35 and inhibits tumor growth.

Furthermore, combinational use of an LSD1 inhibitor and anti-PD-1 therapy can significantly eradicate poorly immunogenic lung cancer with low Trim35. These findings strongly suggest that Trim35 is a promising biomarker for prediction of immunotherapy outcome in NSCLC.

These observations reveal the oncogenic function of IRF5 in the progression of HCC by enhancing glycolysis, further supporting the potential of IRF5 as a viable target for HCC therapy.

Mechanistic analyses indicated that TRIM35 regulates the transition of tetramers and dimers of pyruvate kinase M2 (PKM2) through ubiquitination and thereby affects the Warburg effect. In conclusion, the present results indicated that TRIM35 regulates the tetramer and dimer transition of PKM2 through ubiquitination and affects the malignant biological behavior of breast cancer by modulating the Warburg effect.