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Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
miR-182 induces cervical cancer cell apoptosis through inhibiting the expression of DNMT3a
Jinbao Sun1, Jianghai Ji1, Gaoxiang Huo1
1Department of Gynecology, People's Hospital Cangzhou 061000, Hebei, China.
Abstract:
Cervical cancer is the second most common and malignant tumor among women worldwide. However, the effective therapies for this deadly disease are limited because the elaborate molecular mechanism of progress of cervical cancer remains largely unknown. In present study, we not only determine the miR-182 as an anticancer miRNA molecule but also provide the mechanistic link between miR-182 and its anticancer activity. Primarily, the expression of miR-182 is significantly down-regulated in cervical tumor in contrast to normal cervical tissue, and then miR-182 mimic-treated cell presents reduction of cell proliferation and promoting apoptosis. During this process, DNA methyltransferase 3a (DNMT3a) expression is markedly decreased, thereby likely contributing to miR-182-induced apoptosis. Consistently, over-expression of DNMT3a inhibits the miR-182-induced apoptosis, and inhibition of DNMT3a promotes cervical cancer cell apoptosis, which further demonstrated that DNMT3a involved in cervix carcinogenesis. Collectively, we have revealed a valuable mechanism by which down-regulation of DNMT3a contributes to the miR-182-induced cervical cancer cell apoptosis, which raise a becoming potential that miR-182 administration or inhibition of DNMT3a expression may be the underlying strategies for therapeutic intervention in cervical carcinoma.
Insights
MicroRNA-182 (miR-182) acts as an anticancer molecule in cervical cancer by inhibiting DNA methyltransferase 3a (DNMT3a). Down-regulation of DNMT3a promotes cancer cell apoptosis, suggesting miR-182 or DNMT3a inhibition as potential therapies.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Cervical cancer is a leading cause of cancer death in women globally.
- Limited effective therapies exist due to poorly understood molecular mechanisms of cervical cancer progression.
Purpose of the Study:
- To identify microRNA-182 (miR-182) as a tumor suppressor in cervical cancer.
- To elucidate the molecular mechanism linking miR-182 to its anticancer activity, focusing on DNA methyltransferase 3a (DNMT3a).
Main Methods:
- Quantitative analysis of miR-182 expression in cervical tumor versus normal tissues.
- In vitro studies using miR-182 mimics and DNMT3a manipulation in cervical cancer cells.
- Assessment of cell proliferation, apoptosis, and DNMT3a expression levels.
Main Results:
- miR-182 expression was significantly downregulated in cervical tumors.
- miR-182 mimic treatment reduced cell proliferation and increased apoptosis.
- DNMT3a expression decreased following miR-182 mimic treatment, correlating with enhanced apoptosis.
- Overexpression of DNMT3a counteracted miR-182-induced apoptosis, while DNMT3a inhibition promoted apoptosis.
Conclusions:
- Downregulation of miR-182 is implicated in cervical carcinogenesis.
- The mechanism involves miR-182-mediated suppression of DNMT3a, leading to apoptosis.
- miR-182 administration or DNMT3a inhibition presents potential therapeutic strategies for cervical cancer.
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