Targeting MUC1-C reverses the cisplatin resistance of esophageal squamous cell carcinoma and .

Background: The efficacy of chemotherapeutic treatment of esophageal squamous cell carcinoma (ESCC) is limited by drug resistance during. This severely compromises the long-term survival rate of patients. Therefore, reversing chemotherapy resistance in ESCC may improve the therapeutic outcome.

Inhibition of MUC1-C regulates metabolism by AKT pathway in esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma (ESCC) is one of the most common digestive tumors worldwide. The Mucin 1 (MUC1) heterodimeric protein has been confirmed that is overexpressed in ESCC and induced adverse outcomes. However, the detailed mechanism(s) remained challenging.

Blocking FGFR4 exerts distinct anti-tumorigenic effects in esophageal squamous cell carcinoma.

Background: The FGFR family can be activated by FGFs and plays important roles in regulating cell growth, differentiation, migration, and angiogenesis. Recent studies have suggested that FGFR4 could regulate several processes, including tumor progression. Esophageal squamous cell carcinoma (ESCC) is a malignancy with high global occurrence.

CEP55 promotes the proliferation, migration and invasion of esophageal squamous cell carcinoma via the PI3K/Akt pathway.

Background: Centrosomal protein 55 (CEP55) is an important prognostic biomarker that plays an essential role in the proliferation, migration and invasion of multiple tumors. We aimed to investigate the prognostic value of CEP55 in pN0 esophageal squamous cell carcinoma (ESCC) and explore its biological function in ESCC cells.

Methods: We used immunohistochemistry and Western blot analysis to detect the expression of CEP55 in ESCC.

Inhibition of MUC1-C entering nuclear suppresses MYC expression and attenuates malignant growth in esophageal squamous cell carcinoma.

Background: The mucin 1 (MUC1) heterodimeric protein (N-terminal subunit and C-terminal subunit) is aberrantly overexpressed in esophageal squamous cell carcinoma (ESCC) and has been linked to poor outcomes in this disease. The detailed mechanism(s), however, remains unclear. In this article, we investigate the effects of the MUC1 C-terminal transmembrane subunit (MUC1-C) through the inhibitor GO-201, which inhibits MUC1-C targeting to nuclear.