SNAI1 (Snail Family Transcriptional Repressor 1)

Their disruption facilitates EMT activation and metastatic progression. By integrating recent findings, this review highlights the dual degradative control of Snail and its implications for cancer biology, providing a conceptual framework for therapeutic approaches aimed at restoring degradative balance and limiting metastasis.

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.

We identified three new major downstream targets of Snail1 that improve our understanding of the role of EMT in limiting stress signaling, apoptosis, and senescence during cell cycle suppression to create a vulnerability for therapeutic targeting.

In conclusion, IL-7 induces EMT to promote growth and metastasis NSCLC via the activation of Notch1/TGF-β pathway. IL-7 may be a potential target against human NSCLC.

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On the other hand, in vivo experiments revealed that brexpiprazole significantly inhibited the formation of CRC lung metastases, suppressed the expression of SREBP1(m), SNAI1and MMP9, and upregulated the expression of E-Cad and ZO1. Brexpiprazole inhibits the migration, invasion and metastasis of CRC cells by inhibiting the SREBP1/SNAI1 signalling pathway and downregulating the expression of EMT-related factors.

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.

Our findings suggest CSRS score and its constituent genes represent potential biomarkers for prognosis and immunotherapeutic benefit in COAD patients. Extending this nine-gene set into a broader senescence-associated panel should be a next step toward delivering truly individualized treatment plans.

While the panel showed promising performance for distinguishing MRD-positive from MRD-negative samples, the limited MRD-positive cohort size (n = 11) indicates that validation in larger MRD-focused studies is required before clinical implementation for treatment monitoring. This dPCR-based platform provides accessible, quantitative detection without requiring knowledge of clonal shifts or specific genomic landscape, offering potential advantages for resource-limited settings such as those represented in our Mexican pediatric cohort.

CAFs promote HNSCC progression through IL-32-mediated enhancement of invasion, EMT induction, and CSC properties. Targeting IL-32 signalling may represent a promising therapeutic approach to improve outcomes in HNSCC.

Furthermore, we find that mH4, a specific inhibitor of proteolyzed Talin1, reduces Snail-induced neurite outgrowth and AKT activation within neurons. Overall, Snail may promote cancer-nerve interactions via Talin1, indicating that Talin1 inhibitors can be a potent targeted therapy in malignant tumors with neurite outgrowth.

Importantly, inhibition of ATR in tumors undergoing EMT reduces tumor growth and metastasis, suggesting that ATR inhibition eliminates cancer cells in transition. Thus, during EMT, ATR not only protects genome integrity but also enables transcription reprogramming, revealing that ATR is a safeguard of cell-state transitions and a target to suppress tumor plasticity.