SNAI2 (Snail Family Transcriptional Repressor 2)

Wnt pathway activator SKL2001 and inhibitor LGK974 confirmed KIF20A's role in tumor progression...ChIP-seq and promoter assays verified FOXK1's direct binding to the KIF20A promoter, activating its transcription. In conclusion, KIF20A serves as a diagnostic and prognostic biomarker promoting HCC progression via Wnt/β-catenin signaling, regulated by FOXK1, offering new therapeutic targets.

LRIG3 inhibits hypoxia-induced VM in glioma by facilitating the proteasomal degradation of Snail2 via ubiquitination.

Targeting EMT directly is an appealing idea, and a few strategies are being tested. Whether reversing EMT or stabilizing epithelial features will make standard therapies more effective is not yet settled, but the possibility is driving new interest in combination approaches for ovarian cancer.

Taselisib reversed FAM64A-induced EMT and malignant phenotypes. FAM64A drives BLCA progression via PI3K/mTORC2/AKT-mediated EMT, serving as a potential prognostic biomarker and therapeutic target for metastatic BLCA.

Chemoproteomic and biophysical analyses reveal that erianin targets P4HA1 at the Arg379 site within the α-ketoglutarate (α-KG) binding pocket, leading to downregulation of the HIF1α/SNAIL/SLUG pathway, thereby restoring endothelial integrity by stabilizing VE-cadherin-mediated junctions and upregulating ICAM1 to enhance T-cell adhesion. These findings highlight erianin's potential to overcome vascular barriers and reprogram the tumor microenvironment, providing a novel therapeutic strategy to enhance immunotherapy in GBM and other solid tumors.

Future research should focus on elucidating the spatiotemporal dynamics of these mechanisms and integrating immunotherapy with molecular targeting to improve outcomes for PC patients with hepatic metastasis. This review aims to provide a reference for the mechanism research and therapeutic intervention of hepatic metastasis of pancreatic cancer (HMPC).

This study suggests that eupatolitin suppresses, at least partially, the migration and invasion of oral cancer cells by promoting p38 phosphorylation and downregulating cathepsin S and cathepsin B expression. The findings provide experimental evidence supporting the antimetastatic potential of eupatolitin. Nonetheless, further studies are required to confirm its translational relevance.

Our data further indicate that xenografting can induce significant cellular reprogramming. Comprehensive characterization of ovarian cancer cell-derived xenograft is therefore essential, as they represent a valuable translational platform for investigating therapy adapted ovarian cancer cells.

Our findings suggest that DMBX1 may have potential as a prognostic biomarker for prognostic assessment in colon cancer and is associated with alterations in the tumor immune microenvironment.Mechanistically, DMBX1 likely primarily influences the occurrence and development of colon cancer by promoting the invasion and migration of colon cancer cells.

These findings provide both mechanistic insights and experimental validation for the potential application of ARE as a radiosensitizer in colorectal cancer radiotherapy.

Supratentorial ependymomas with ZFTA-RELA fusions represent a highly aggressive pediatric brain tumor subtype, yet the post-transcriptional mechanisms driving their malignancy remain unclear. This study fills a critical gap by systematically profiling miRNA expression in fusion-positive and fusion-negative supratentorial ependymomas, revealing a distinct fusion-associated miRNA signature. The identification of hsa-miR-138-5p upregulation and hsa-miR-135b-5p/hsa-miR-216a-3p downregulation, converging on key oncogenic nodes such as TERT, YAP1, RELA, and TP53, provides novel mechanistic insight into how fusion-driven miRNA dysregulation enhances epithelial-mesenchymal transition and stemness. The findings suggest that miRNA-fusion interactions play an important role in tumor aggressiveness and highlight hsa-miR-138-5p as a potential biomarker for disease progression. Clinically, the work advances understanding of fusion-driven ependymoma biology and lays the foundation for developing miRNA-based diagnostic and therapeutic strategies targeting molecular mechanisms of tumor progression.

Our findings suggest that miR-20a-5p plays an oncogenic role in luminal breast cancer by promoting EMT, while MALAT1 may contribute to disease progression through indirect regulatory mechanisms. Finally, MALAT1 and miR-20a-5p might serve as potential therapeutic and prognostic targets in LBC.