TIMP3 (TIMP Metallopeptidase Inhibitor 3)

TIMPs display contrasting expression profiles and distinct pathway associations in breast cancer. TIMP1 emerges as the only consistently overexpressed inhibitor, while TIMP4 appears as a promising prognostic marker with unique MMP correlations that may influence tumor behaviors.

For perturbation, the EZH2 inhibitor tazemetostat was evaluated in the CRPC-relevant C42 cell line with H3K27me3 readouts and transcriptomic profiling, with key changes validated by RT-qPCR...This multi-layer integrative analysis suggests that EZH2 is associated with proliferative malignant states and immunosuppressive microenvironment features in advanced PCa, including Treg-linked crosstalk. Transcriptomic profiling following EZH2 inhibition supports modulation of these programs by EZH2-targeted perturbation, while functional and causal mechanisms warrant further investigation.

These findings uncover a complex regulatory role for HIF-1α in bladder cancer and identify TIMP3 as a critical mediator of its effects. Further studies are warranted to elucidate the transcriptional regulation of TIMP3 by HIF-1α and to validate its role in vivo, which may contribute to the advancement of targeted therapeutic strategies for bladder cancer.

Effect size estimates were relatively large for both the group effect (partial η2=0.20) and the time x group interaction (partial η2=0.24), suggesting that the study may have been underpowered to detect this difference statistically. In conclusion, the present exploratory study suggests that suramin exerts a dual antitumor effect on tongue squamous cell carcinoma by suppressing proliferative transcriptional programs, and modulating extracellular and stress response pathways, providing a basis for future studies to further elucidate its therapeutic relevance.

The most frequent methylation related microRNA was miR-296, followed by miR-193 and miR-137. This study for the first time elucidated the scientometric characteristics of all the publications on methylation modification in oral carcinogenesis, and would provide new insights for researchers to comprehend the methylation specific gene profile related OPMD/OSCC.

Cross-organ single-cell integration prioritizes liver-selective stromal circuitry and nominates hepatocyte-FB axes (HGF-MET, AGT-AGTR1B) as plausible links between fibrogenic remodeling and a pro-tumorigenic niche, yielding testable hypotheses at the interface of regeneration, RAS biology, and tumor initiation.

Collectively, these findings establish a mechanistic axis in which miR-149-3p-mediated suppression of TIMP3 promotes sorafenib resistance, EMT, and stemness in HCC. This work identifies TIMP3 as a pivotal determinant of tumor aggressiveness and suggests restoring TIMP3 or targeting downstream pathways as strategies to overcome resistance.

Clinical validation using TCGA data confirmed elevated RBP-J and miR-188-5p expression, alongside reduced TIMP2/3 levels, as prognostic biomarkers for poor CRC outcomes. These findings reveal a novel Notch-miR-188-5p-TIMP2/3 signaling cascade driving exosome-mediated PMN formation, offering insights into therapeutic strategies targeting the metastatic microenvironment.

The study demonstrates that the MMP-TIMP-miRNA axis exhibits subtype-specific expression patterns in the BC cell lines. The observed heterogeneity highlights the importance of post-transcriptional regulation and suggests that integrated profiling of MMPs, TIMPs, and regulatory miRNAs may provide novel insights into the invasive potential of BC and identify candidate biomarkers for clinical validation.

Cellular experiments further corroborated the regulatory effect of let-7c-5p on Timp-3. Overall, these results suggest that exercise promotes Timp-3 expression by downregulating let-7c-5p carried by circulating exosomes, thereby mitigating atherogenesis and vascular inflammation in ApoE-/- mice.

Additionally, nano-curcumin induces apoptosis and inhibits migration. These findings suggest the nano-curcumin and tamoxifen combination may be a promising therapeutic strategy to overcome drug resistance in ER+ breast malignancies.