PTC209, a Specific Inhibitor of BMI1, Promotes Cell Cycle Arrest and Apoptosis in Cervical Cancer Cell Lines
Autor: | Ming Poi, Junan Li, Zachary VanGundy |
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Rok vydání: | 2019 |
Předmět: |
Cancer Research
Cell Survival Uterine Cervical Neoplasms Apoptosis Biology HeLa 03 medical and health sciences 0302 clinical medicine Cancer stem cell Cell Line Tumor medicine Humans Viability assay Enzyme Inhibitors Cell Proliferation Polycomb Repressive Complex 1 Cervical cancer Oncogene HPV infection Cell Cycle Checkpoints General Medicine Cell cycle medicine.disease biology.organism_classification Gene Expression Regulation Oncology 030220 oncology & carcinogenesis Cancer cell Neoplastic Stem Cells Cancer research Female |
Zdroj: | Anticancer Research. 40:133-141 |
ISSN: | 1791-7530 0250-7005 |
DOI: | 10.21873/anticanres.13934 |
Popis: | BACKGROUND/AIM Aberrant expression of the BMI1 oncogene has been prevalently found in a variety of human cancers, including cervical cancer. Recent studies have shown that PTC209, a specific BMI1 inhibitor, exhibits high potency in inhibiting the growth of colon, breast, oral cancer cells and cancer-initiating cells, indicative of its chemotherapeutic potential. In the current study, we evaluated the inhibitory abilities of PTC209 in cervical cancer cells. MATERIALS AND METHODS Three cervical cell lines, C33A, HeLa, and SiHa were treated with PTC209. The impacts of PTC209 on BMI1 were investigated using quantitative reverse-transcription PCR assay (qRT-PCR) and western blotting; changes in cell viability, cell cycle distribution, and apoptosis were assessed using cell viability testing, colony formation assay and flow cytometry analyses, respectively. RESULTS PTC209 exhibited considerably high short-term and long-term cytotoxicities in all tested cervical cancer cell lines regardless of their HPV infection status, TP53 and pRb statuses. PTC209 significantly downregulated the expression of BMI1 in cervical cancer cell lines, and such downregulation led to G0/G1 arrest (p |
Databáze: | OpenAIRE |
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