Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.4.2.30 (PARP)
 13,611 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A previous study has reported that frequent amplifications of the TG-interacting factor (TGIF) were observed in esophageal squamous cell carcinoma. The aim of the present study was to investigate the potential role of TGIF in the proliferation and tumorigenicity of the esophageal cancer cell line EC109 and cisplatin-induced apoptosis. Stable TGIF-knockdown EC109 cell line was established by infecting short hairpin RNA (shRNA) lentiviral particles. Soft agar and tumor xenograft assays were applied in nude mice. Flow cytometry was employed to evaluate the cell cycle and apoptosis. Western blot analysis was used to detect the expression of proteins. TGIF knockdown suppressed EC109 cell proliferation, colony formation in soft agar and tumor growth in nude mice, induced cell cycle arrest in the G1 phase, and promoted cisplatin-induced apoptosis. In addition, TGIF knockdown significantly reduced the expression of phospho-Rb in EC109 cells. The reduced level of full length PARP expression and the increased level of cleaved caspase-3 expression were observed in EC109 cells with the treatment of cisplatin and TGIF knockdown. The results suggest that knockdown of TGIF attenuated the proliferation and tumorigenicity of EC109 cells, and promoted cisplatin-induced apoptosis.
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PMID:Knockdown of TGIF attenuates the proliferation and tumorigenicity of EC109 cells and promotes cisplatin-induced apoptosis. 2934 16

The present study was designed to explore the sensitivity of MDA-MB-231 cells to cisplatin after silencing the expression of TG-interacting factor (TGIF) protein. Cell viability was measured using an MTT assay. Cell apoptosis was detected by the annexin V and dead cell assay and the Hoechst staining assay. Protein expression was analyzed using western blot analysis. A colony formation assay was also performed. It was observed that cisplatin reduced the expression of TGIF protein in a dose- and time-dependent manner. Silencing TGIF significantly suppressed the cell proliferation and colony formation in MDA-MB-231 cells with the treatment of cisplatin. Results indicated that silencing TGIF could dramatically increase the cisplatin-induced apoptosis rate in MDA-MB-231 cells. The expression of PARP and caspase-3 proteins was correlated with the effect that silencing TGIF enhanced cisplatin sensitivity in MDA-MB-231 cells. The present data showed that silencing TGIF promoted apoptotic sensitivity that was induced by cisplatin in MDA-MB-231 human breast cancer cells and suggested that TGIF might be a therapeutic target for improving the chemotherapy response in triple-negative breast cancer.
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PMID:Silencing of TGIF sensitizes MDA-MB-231 human breast cancer cells to cisplatin-induced apoptosis. 2945 3