Magic™ Anti-GATA3 (phospho S308) polyclonal antibody

Background. Long noncoding RNAs (lncRNAs) have been known to play important roles in the progression of various types of human cancer. LncRNA GATA3 antisense RNA 1, GATA3-AS1, has been reported to be associated with T-cell development and differentiation. However, the expression pattern and function of GATA3-AS1 in hepatocellular carcinoma (HCC) remain unknown. Methods. Real-time quantitative PCR (RT-qPCR) assay was conducted to detect GATA3-AS1 expression levels in 80 cases of pairs HCC tissues and matched normal tissues. Chi-squared (chi(2)) test was used to analyze the correlation between GATA3-AS1 expression and clinicopathologic variables. Survival curves were plotted using the Kaplan-Meier method and were compared via the log-rank test. The cell counting kit-8 (CCK-8) and wound scratch assays were applied to detect the effect of GATA3-AS1 knockdown and overexpression on cell growth and migration of HCC. RT-qPCR was performed for the detection of the phosphatase and tensin homolog (PTEN), cyclin-dependent kinase inhibitor 1A (CDKN1A), and tumor protein p53 (TP53) expression in HCC cells after GATA3-AS1 knockdown and overexpression. Results. GATA3-AS1 was significantly upregulated in HCC tissues compared with matched normal tissues. The high expression of GATA3-AS1 was significantly correlated with larger tumor size, advanced TNM stage, and more lymph node metastasis. High GATA3-AS1 expression was markedly correlated with shorter overall survival times of HCC patients. Furthermore, knockdown of GATA3-AS1 obviously inhibited Hep3B and HCCLM3 cell growth and migration, whereas overexpression of GATA3-AS1 had the opposite effects. In addition, GATA3-AS1 knockdown resulted in upregulated expression levels of tumor-suppressive genes, PTEN, CDKN1A, and TP53, in Hep3B and HCCLM3 cells, while restoration of GATA3-AS1 decreased PTEN, CDKN1A, and TP53 expression levels. Conclusion. Our data suggested that GATA3-AS1 promotes cell proliferation and metastasis of HCC by suppression of PTEN, CDKN1A, and TP53.

The long-term risk of secondary malignancy is a potential late effect of brachytherapy. However, the time interval, anatomic site and histopathology are not well studied. We sought to characterize the bladder cancers that developed following treatment of prostate cancer with brachytherapy. Between 1998 and 2014, 4570 patients were treated with brachytherapy at the BC Cancer Agency. Out of those, 69 patients subsequently developed bladder cancer, some of which could have been radiation induced. Histology slides were reviewed for all cases, and site and pathologic features were recorded. Cases were classified as luminal and basal subtypes based on GATA3 and CK5/6 immunohistochemistry. Bladder neck and trigone were among the common sites of involvement. Pathologic review of cases showed that 68 % were high-grade, 25 % were muscle-invasive, and 20 % showed variant histology, including small cell carcinoma, sarcomatoid carcinoma, squamous cell carcinoma, and adenocarcinoma. A subgroup of cases more likely to be radiation-induced, based on site and time interval, was associated with increased pathologic stage (pT1 or higher) compared to the other cases (70 % vs 34 %, p = 0.01). In conclusion, the majority of bladder cancers following brachytherapy in this cohort were of high grade and low stage at diagnosis, most of them demonstrating luminal immunophenotype. A significant number of variant histologies are seen, each demonstrating a specific immunophenotype.