ZEB2 (Zinc Finger E-Box Binding Homeobox 2)

Elevated mRNA levels of EMP3, THBS2, and ITGA5 were significantly correlated with poorer overall survival. Fn and Pg can promote invasive phenotypes in CRC through distinct mechanisms, each modulating a unique subset of p-EMT and without instigating a complete, coordinated EMT gene signature.

Our research reveals a novel mechanism by which ESRP2 affects BC metastasis through post-transcriptional regulation. ESRP2 may present as a promising biomarker in combating BC cell migration by targeting EMT.

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.

These results identify MMP9, TWIST2, ZEB2, and WNT11 as promising biomarkers for overcoming chemoresistance in HGSOC. Further functional validation of these genes is needed to confirm the biological significance of the observed correlations.

The intertwined ETAR/GSDME/ZEB1 circuitry characterizes mesenchymal HG-SOC patients and associates with a high-risk of poor survival. Together, these findings unveil GSDME as a key transcriptional regulator of aggressive behaviors and worse prognosis in HG-SOC patients, in an ET-1-driven alliance with ZEB1, which could be targeted by ET-1R antagonist to reduce the metastatic burden of this tumor.

The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 29: 1579‑1587, 2013; DOI: 10.3892/or.2013.2267].

These insights may enhance our understanding of the mechanisms driving colorectal cancer progression and identify potential therapeutic targets for aggressive disease.

Four antisense genes, namely HOXA10-AS, LEF1-AS1, MSC-AS1, and ZEB2-AS1, have been clinically cross-validated and have consistently demonstrated to be associated with patient outcomes in multiple independent cohorts by different research teams, with clear evidence for the prioritization of clinical biomarker development in HNC. Single nucleotide polymorphisms (SNPs) of antisense genes with evidence for HNC risk or outcomes should be further validated in different ethnic groups, for potential global HNC applications.

Senescent TAMs influence NB immunosuppression and progression. EIF5 is a key regulator of TAM senescence and a potential therapeutic target. Our risk model may guide clinical stratification and targeted interventions.

Overexpression of EMT transcription factors SNAI1 and ZEB1 reflect more aggressive histopathological patterns of PDAC. The strong correlation of SNAI1 expression with the expression of other EMT-TFs highlights its' role in peripancreatic invasion, as well as impact on overall survival and may serve as an argument defining the leading role of SNAI1 in this context.

Moreover, pseudotime trajectory analysis demonstrated that cisplatin treatment modulates a CSC-like phenotype differently in cells grown as monolayer versus tumorsphere. Our findings provide important insights into the role of cisplatin in NSCLC and highlight potential targets within the lung cancer microenvironment.

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.