<i>MALAT1</i> Inhibits Proliferation of HPV16-Positive Cervical Cancer by Sponging miR-485-5p to Promote Expression of <i>MAT2A</i>

Abstract

Cervical cancer is the leading cause of morbidity and mortality in women throughout the world, human papillomavirus 16 (HPV16) is the main type of HPV causing invasive cervical cancer. However, the underlying mechanism of the high carcinogenicity of HPV16 remains unclear. In the current study, we documented that metastasis-associated lung adenocarcinoma transcript 1 (<i>MALAT1</i>), a long noncoding RNA, is upregulated in HPV16-positive cervical cancer tissue and cell lines. The results of immunohistochemistry and immunofluorescence showed that <i>MALAT1</i> was mainly localized in the cytoplasm. To clarify the biological functions of <i>MALAT1</i> in cervical cancer cells, we performed gain- and loss-of-function experiments to explore the underlying molecular mechanism. Functionally, the proliferation of cervical cancer was detected by Cell Counting Kit-8 (CCK-8) and colony formation assay in <i>MALAT1</i> overexpression or knockdown cells, our data showed that <i>MALAT1</i> promotes the proliferation of cervical cancer cells. Mechanistically, our results suggested that <i>MALAT1</i> upregulates Methionine adenosyltransferase 2A (<i>MAT2A</i>) by sponging miR-485-5p. Moreover, the gain-of-function assay validated the function of <i>MAT2A</i> in HPV16-positive cervical cancer proliferation. Taken together, our results demonstrated that <i>MALAT1</i> acts as a competitive endogenous RNA (ceRNA) to regulate <i>MAT2A</i> by sponging miR-485-5p in HPV16-positive cervical cancer, suggesting that <i>MALAT1</i> may act as a potential therapeutic target for HPV16-positive cervical cancer.