Recent studies have uncovered an important post-transcriptional effect of m 6A, which is the triggering of microRNA (miRNA) biogenesis ( 10).
Accumulating evidence indicates that m 6A regulates RNA metabolism, including mRNA translation, degradation, splicing, export, and folding. m 6A is necessary for a myriad of physiological processes, such as cell status regulation, sex determination, and development ( 7– 9). One ubiquitously occurring epigenetic modification is mediated by N 6-methyladenosine (m 6A), which methylates the adenosine N 6-position in mammalian mRNA ( 6). Gene expression has been noted to be strongly influenced by RNA modification, thereby leading to the development of the new field of RNA epigenetics ( 5). Therefore, the identification of novel therapeutic methods is critical, and inevitably requires a deeper grasp of cervical cancer biology. 5-year survival rates upon relapse remain dismal at only 30–60% ( 3, 4). Among these groups of patients, relapse rates exceeding 50% after standard treatments have been documented. However, there remains a substantial risk of tumor relapse in patients who develop locally advanced cervical cancer with high risks such as positive lymph nodes or positive surgical margins. Most patients respond to standard treatments which include surgery and radiotherapy. Nearly 90% of deaths occurred in developing countries, and more than half of these were recorded in Asia ( 2). Reintroduction of miR-193b profoundly inhibits tumorigenesis of cervical cancer cells both in vivo and in vitro through CCND1 targeting.Ĭonclusions: m 6A associated downregulation of miR-193b promotes cervical cancer aggressiveness by targeting CCND1.Ĭervical cancer is a frequently encountered gynecological malignancy as a primary cause of cancer-associated mortality in women ( 1). METT元 modulates miR-193b mature process in an m 6A-dependent manner. miR-193b functions as a tumor suppressor that is regulated by m 6A methylation in cervical tumors.
Results: Our study suggested that lower miR-193b expressions were strongly linked to more advanced cervical cancer stages and the presence of deeper stromal invasion. Luciferase reporter assays, qRT-PCR, and Western blotting were enlisted to study the interaction between miR-193b and CCND1. The CCK-8 assay, cell cycle analysis, qRT-PCR, Western blot assay, IHC, RIP, and xenograft models were utilized to explore the impact of miR-193b in cervical cancer and how m 6A regulates miR-193b expression. Methods: Cervical cancer samples and the matching adjacent normal cervical tissues were used to determine the significance of miR-193b in cervical cancer. This study focuses on how miR-193b promotes cervical cancer aggressiveness as well as the role of m 6A in miR-193b silencing. Objective: Cervical cancer is a frequently encountered gynecological malignancy as a major contributor to cancer-related deaths in women.
2Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.1Department of Gynecological Oncology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.Chunxian Huang 1,2†, Jinxiao Liang 1,2†, Shaodan Lin 1,2, Dongyan Wang 1,2, Qingsheng Xie 1,2, Zhongqiu Lin 1,2* and Tingting Yao 1,2*
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