Long non-coding RNA ABHD11-AS1 facilitates the progression of cervical cancer by competitively binding to miR-330–5p and upregulating MARK2

基因敲除 生物 下调和上调 癌变 癌症研究 反义RNA 长非编码RNA 细胞生长 核糖核酸 细胞 小RNA 细胞凋亡 免疫印迹 分子生物学 癌症 基因 遗传学
作者
Shunyu Hou,Xiaoqian Zhang,Jian Yang
出处
期刊:Experimental Cell Research [Elsevier BV]
卷期号:410 (1): 112929-112929 被引量:11
标识
DOI:10.1016/j.yexcr.2021.112929
摘要

Cervical cancer (CC) is among the most prevalent gynecological malignancies. Participation of long non-coding RNA (lncRNA) in modulating biological behaviors of CC cells has been confirmed. However, the function of lncRNA ABHD11 antisense RNA 1 (ABHD11-AS1) in CC is still unclear. RT-qPCR and Western blot were performed for measuring RNA and protein levels. Functional assays were done to evaluate ABHD11-AS1 influences on cell proliferation, apoptosis, invasion and migration. After the verification of ABHD11-AS1 distribution in CC cells, mechanism assays were conducted to study the interaction of relative RNAs. ABHD11-AS1 expression was abnormally high in CC cells. In vitro experiments showed ABHD11-AS1 downregulation restrained CC cell malignant phenotypes. In vivo experiments proved ABHD11-AS1 knockdown impeded tumor growth. Moreover, miR-330-5p was corroborated to bind with ABHD11-AS1 in CC cells and microtubule affinity regulating kinase 2 (MARK2) was confirmed to be targeted by miR-330-5p. MiR-330-5p inhibition or MARK2 overexpression could countervail the suppressive effect of ABHD11-AS1 knockdown on CC cell malignant behaviors. We found that ABHD11-AS1 facilitated CC tumorigenesis through competitively sequestering miR-330-5p to upregulate MARK2, indicating ABHD11-AS1 as a potential biomarker in CC.
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