p120-Catenin Downregulation and PIK3CA Mutations Cooperate to Induce Invasion through MMP1 in HNSCC
In conclusion, this study demonstrates that P120CTN downregulation and PIK3CA mutations promote MMP1-driven invasion, providing a potential novel target for limiting metastasis in HNSCC. Implications: Because of its role in invasion, MMP1 represents a novel, potential target for limiting metastasis in a subset of HNSCCs with P120CTN downregulation and PIK3CA mutations. Mol Cancer Res; 15(10); 1398–409. ©2017 AACR.
ConclusionTERT promoter mutations are most likely a late event in tumor development, occurring in a context of critically short telomeres, mostly in patients with oral cavity SCC.TERT levels, but notTERT promoter mutational status impact clinical outcome.
Conclusions: These data suggest that lack of HPV infection is associated with more prominent activation of Wnt/βCatenin signaling pathway and gain of stem-like traits in tobacco-related OSCCs. PMID: 31929745 [PubMed - in process]
Authors: Bai S, Yan YB, Chen W, Zhang P, Zhang TM, Tian YY, Liu H Abstract High-throughput gene expression profiling has recently emerged as a promising technique that provides insight into cancer subtype classification and improved prediction of prognoses. Immune/inflammatory-related mRNAs may potentially enrich genes to allow researchers to better illustrate cancer microenvironments. Oral cavity squamous cell carcinoma (OC-SCC) exhibits high morbidity and poor prognosis compared to that of other types of head and neck squamous cell carcinoma (HNSCC), and these differences may be partially due to differences withi...
Formononetin induces apoptotic cell death through the suppression of mitogen‑activated protein kinase and nuclear factor‑κB phosphorylation in FaDu human head and neck squamous cell carcinoma cells. Oncol Rep. 2019 Dec 13;: Authors: Oh JS, Kim TH, Park JH, Lim H, Cho IA, You JS, Lee GJ, Seo YS, Kim DK, Kim CS, Yu SK, Kim HJ, Kim SG, Kim JS Abstract Formononetin, a phytoestrogen extracted from various herbal plants, has been investigated as an anticancer agent against diverse types of cancer. The aim of the present study was to investigate the induction of apoptotic cell death by formononetin ...
AbstractWe performed a prospective trial to assess the clinical benefit of a tailored gene set built on a next-generation sequencing (NGS) platform in patients with recurrent or metastatic head and neck squamous cell carcinoma (HNSCC). Archived tumor tissue obtained from patients with recurrent or metastatic HNSCC was analyzed for variants by a tailored Comprehensive Cancer Gene set of 40 genes (CCG-40) performed on a NGS platform. These data were provided to clinicians to inform treatment decisions. The primary endpoint was clinical benefit (disease control) that resulted from selection and administration of a targeted th...
In conclusion, our results suggest that UBE2C is consistently upregulated in many human solid tumors. It promotes HNSCC progression and may serve as a potential prognostic biomarker in HNSCC. Future studies are warranted to unveil the underlying molecular pathways of UBE2C in HNSCC. PMID: 31870550 [PubMed - as supplied by publisher]
CONCLUSIONS: The clinical study of CXCR1/2 inhibitors in combination with adoptively transferred NK cells is warranted. PMID: 31848188 [PubMed - as supplied by publisher]
ConclusionsThe nonphosphorylatable Y602 F-EPS8 and 4 F-EPS8 mutants decreased the expression of EPS8 downstream targets, as well as reducing tumor cell growth and motility, implying a crucial role for phosphorylation of EPS8, principally at Y602, in mediating protumorigenic signal transduction.
This study aimed to access the prognostic value of CCR1, CCR3, CCR4, CCR5, CCR7, and CXCR4 in head and neck squamous cell carcinomas.
Epidermal growth factor receptor pathway substrate 8 (EPS8) is a scaffolding protein involved in regulating cell proliferation, actin dynamics, and receptor trafficking in human cells. EPS8 expression is increased in a range of human cancers, including head and neck squamous cell carcinoma (HNSCC). Previous studies have indicated that overexpression of EPS8 enhances mitogenesis and migration of tumor cells and is sufficient to convert nontumorigenic cells to a tumorigenic phenotype. The nonreceptor tyrosine kinase Src is reported to phosphorylate EPS8 at 4 tyrosine residues, although the impact of this on EPS8 function is unknown.