Human FSTL1 blocking peptide

The aim of this study is to identify the genetic alteration in SPARC gene family and its association with head and neck squamous cell carcinoma (HNSCC). Head and neck cancer is a set of cancerous lesions arising from the squamous cell of the mucous membrane of the oral cavity, nose throat, larynx and pharynx. SPARC gene encodes for cysteine rich acid matrix metalloprotein, osteonectin whose expression in metastatic OSCC (Oral squamous cell carcinoma) was found to be higher. This expression pattern also correlated with the worst pattern of invasion and differentiation of OSCC tumors. In line with the above facts, the present study was carried out to ascertain the gene alterations and their consequences. Also the putative association of gene alterations with HNSCC was analyzed using computational tools. The Cancer Gene Atlas (TCGA, Firehose Legacy) dataset hosted by the cBioportal server was used in the present study. The nonsynonymous variants identified were further assessed for protein stability and pathogenicity employing IMutant and PROVEAN tools. Gene amplification was observed in the FSTL1 gene, which was also shown to present with the highest frequency of gene alterations (5%) among eight genes. Furthermore, the expression of the FSTL1 gene was found to differ significantly among different grades of HNSCC. In conclusion, the study throws light on the possible association of the FSTL1 gene of the SPARC family with HNSCC.

This study examined the in-vivo effect of the NSAID celecoxib on DNA methylation in the promoter region of the tumor-suppressor genes cadherin 13, tissue factor pathway inhibitor 12, and follistatin-like protein 1, and on apoptosis, in esophageal squamous cell carcinoma (ESCC). Forty-five patients who underwent an esophagectomy for ESCC were allocated to either a treatment group (n=22) or a control group (n=23). Patients in the treatment group were administered 800mg/day of celecoxib for 14 days before surgery. Patients in the control group did not take any type of NSAID. Biopsies of the tumor were collected before surgery and tissue from the resection specimens after surgery. Methylation-specific PCR was used to measure DNA methylation and apoptosis was measured by flow cytometry. There was no difference in the proportion of patients with methylation for each of the genes between the patient groups before treatment. In those patients with pretreatment methylation, there was a significant reduction in the proportion with methylation and a significant increase in the corresponding messenger RNA expression after treatment with celecoxib. In those tissues in which there was a reduction in methylation following celecoxib treatment, there was a significant increase in the percentage of apoptotic cells, but not in the tissues with no change in methylation. In ESCC, in-vivo treatment with celecoxib is associated with a reduction in DNA methylation and increase in messenger RNA expression of tumor-suppressor genes, and increases in apoptosis.