MiR-34a Inhibits Viability and Invasion of Human Papillomavirus–Positive Cervical Cancer Cells by Targeting E2F3 and Regulating Survivin
Autor: | Xiaohua Song, Hong-hua Yin, Fangling Ning, Qianhua Song, Dianzhong Geng |
---|---|
Rok vydání: | 2015 |
Předmět: |
Human Papillomavirus Positive
Survivin Blotting Western Uterine Cervical Neoplasms medicine.disease_cause Inhibitor of Apoptosis Proteins HeLa Downregulation and upregulation Cell Movement Biomarkers Tumor Tumor Cells Cultured Humans Medicine Neoplasm Invasiveness RNA Messenger Viability assay Cell Proliferation Cervical cancer Human papillomavirus 16 Human papillomavirus 18 biology Reverse Transcriptase Polymerase Chain Reaction business.industry Papillomavirus Infections Obstetrics and Gynecology medicine.disease biology.organism_classification Gene Expression Regulation Neoplastic MicroRNAs Oncology E2F3 Transcription Factor Cancer cell Cancer research Female business Carcinogenesis |
Zdroj: | International Journal of Gynecologic Cancer. 25:707-713 |
ISSN: | 1525-1438 1048-891X |
Popis: | ObjectivePrevious studies confirmed that high-risk human papillomavirus (HR-HPV) infection is a risk factor of cervical cancer, and the infection was associated with significantly reduced miR-34a expression during carcinogenesis. However, the downstream targets of miR-34a and their roles are still not well understood. This study explored the regulative role of miR-34a on E2F3 and survivin expression and the viability and invasion of HPV-positive cervical cancer cells.MethodsMiR-34a and survivin expression in 56 cases of HR-HPV–positive patients, 28 cases of HR-HPV–negative patients, and 28 normal cases without HR-HPV infections were measured. Human papillomavirus-18–positive HeLa cervical cancer cells and HPV-16–positive SiHa cells were used to explore the effect of miR-34a on cell viability and invasion. The molecular target of miR-34a was also explored in cervical cancer cells.ResultsThe results showed that miR-34a overexpression could inhibit HPV-positive cancer cell viability, whereas its downregulation promoted cell viability. E2F3 is a direct target of miR-34a in HPV-positive cervical cancer cells. By targeting E2F3, miR-34a could regulate the expression of survivin. Thus, through regulating E2F3 and survivin, miR-34a could reduce the viability and invasion of HPV-positive cervical cancer cells.ConclusionsThis study confirmed a novel miR-34a–E2F3–survivin axis in the tumor suppressor role of miR-34a in cervical cancer. |
Databáze: | OpenAIRE |
Externí odkaz: |