In conclusion, our study first reported that PTP1B was the positive regulator of EGFR by dephosphorylating MYH9 at Y1408 to promote cell migration and invasion, which revealed the regulatory mechanism of PTP1B-MYH9-EGFR axis in ESCC.
Single Nucleotide Polymorphisms in MicroRNA-Binding Site of Epidermal Growth Factor Receptor Signaling Pathway and Susceptibility to Esophageal Squamous Cell Carcinoma.
Together, our initial findings demonstrate that CGA suppresses ESCC progression, downregulates the expression of BMI1 and SOX2, and provide an anti-tumor candidate for ESCC therapy.
This study determined optimal cutoff values of serum SCC-Ag and CEA concentrations for predicting postoperative recurrence of ESCC, which enabled selection of high-risk patients.
The number of CD8<sup>+</sup> tumour-infiltrating immune cells (TIICs) and PD-1<sup>+</sup> TIICs, and PD-L1 expression on tumour cells (PD-L1<sub>TC</sub>) were immunohistochemically examined in the surface (Surf), centre (Cent) and invasive front (Inv) of tumours surgically resected from 192 patients with ESCC.
In summary, this study revealed that linc-ROR modulated cell apoptosis and regulated p53 ubiquitination via targeting miR-204-5p/MDM2 axis, which provides a novel therapeutic insight into treatments for ESCC.
Keratin 17 (KRT17) upregulation in ESCC cells not only promoted cell proliferation but also increased invasion and metastasis accompanied with AKT activation and epithelial-mesenchymal transition (EMT).
Together, our initial findings demonstrate that CGA suppresses ESCC progression, downregulates the expression of BMI1 and SOX2, and provide an anti-tumor candidate for ESCC therapy.
We investigated the mechanism of angiogenesis in early-stage ESCC by examining the expression of vascular endothelial growth factor (VEGF)-A and chondromodulin (ChM)-1.
Our findings are the first to provide compelling evidence of the role of BRCA2 in ESCC genetic susceptibility in Chinese, suggesting defective homologous recombination is an underlying cause in ESCC pathogenesis, which is amenable to therapeutic options based on synthetic lethality approaches such as targeting BRCA2 with PARP1 inhibitors in ESCC.
A case-control study including 494 ESCC patients and 494 controls was carried out to investigate the genetic susceptibility of 4 microRNA-binding site SNPs (rs712 in the binding site of KRAS to let-7, rs8904 in the binding site of NFBIA to mir-507, rs3738894 in the binding site of protein kinase C epsilon to mir-218, rs701848 in the binding site of phosphatase and tensin to mir-1304) as well as the interactions of gene-environment in the development of ESCC.