TWIST1 (Twist Family BHLH Transcription Factor 1)

Transcriptional (Twist1/NR2F2) and post-transcriptional (miRNA-mediated) regulatory mechanisms were implicated in LIFR-driven pathogenesis. Our study first investigated NF-serum proteomic concordance as a predictor of PR and demonstrated the potential of integrated multi-compartment analysis for predicting recurrence.

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.

Terminal deoxynucleotidyl transferase nick-end-labeling and Ki67 staining also showed that ESPNP short hairpin RNA treatment enhanced cell apoptosis and reduced cell proliferation. Taken together, our study demonstrated that ESPNP promotes GC progression by enhancing proliferation, invasion, metastasis, and epithelial-mesenchyme transition, suggesting its potential as a prognostic biomarker and therapeutic target in GC.

Collectively, our findings identify NARF as stiffness-responsive driver that is transcriptionally regulated by YAP protein in HCC. By activating LEF1-mediated Wnt signaling in an EP300 dependent manner, NARF promotes HCC growth and metastasis, highlighting its potential as a prognostic biomarker and therapeutic target for HCC.

The compensatory expression of Twist1 in FOXP2-overexpressing breast cancer cells counteracted FOXP2's inhibitory effects on the stemness of breast cancer cells. Together, the results showed that FOXP2 attenuated the stemness of breast cancer cells by abolishing the transcription of Twist1.

This study reveals the critical role of FUBP3 in lung cancer metastasis and identifies a new regulatory axis involving FUBP3-STAT3-Twist1. FUBP3 interacts with STAT3, enhancing STAT3-dependent Twist1 expression, which promotes EMT and metastasis. FUBP3 functions as a prognostic biomarker, and STAT3 inhibitors present therapeutic strategies for lung cancer, offering novel insights for precision treatment.

No correlation was observed with vessel-rich (CD31-positive) or fibrous (vimentin-positive) tumor regions. Immunohistochemistry for Twist1 and Snail/Sslug confirmed protein-level expression (n=19), with inter- and intratumoral heterogeneity of EMT markers.Demonstration of Twist1 and Snail/Slug expression in JA indicates involvement of the embryologic process of EMT in JA and supports the embryologic explanatory model, which accounts for the clinical characteristics of this unique fibrovascular neoplasm.

In vivo, xenograft assays in NOD-SCID mice reveal that while phosphorylated Lamin A/C or EZH2 promote tumor growth and metastasis, phospho-deficient mutants markedly suppress it. Lamin A/C-EZH2 interaction regulates the expression of E-M-associated transcription factors, highlighting the role of this interaction in modulating transcriptional plasticity, thereby serving as a potential therapeutic target for regulating metastasis in breast cancers.

β-elemene modulates anoikis and EMT in breast cancer cells via the IGF1/Twist1 signaling pathway, offering novel insights for breast cancer therapy.

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Therefore, knowledge of epigenetics in regulating cancer stem cells via stem cell transcription factors may be a promising solution for the reversal of therapy-resistant BC. In this review, we emphasize stem cell transcription factors, cancer stem cells, and epigenetic regulation as critical drivers of drug resistance in BC.

It induced mitochondrial membrane potential loss and apoptosis, downregulated stemness-related proteins (ALDH1A1, KLF4, and Sox2), and suppressed epithelial-mesenchymal transition markers (Snail, Twist1, Slug, Vimentin, and MMP-9), indicating strong antitumor activity. The recombinant oncolytic adenovirus Ad-VP3 exerts potent antitumor effects on hepatocellular carcinoma cells by inducing mitochondrial dysfunctionmediated apoptosis and impairing stemness and metastatic potential, suggesting its promise as a novel therapeutic strategy for HCC.