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LncRNA SLCO4A1-AS1 promotes colorectal cancer cell proliferation by enhancing autophagy via miR-508-3p/PARD3 axis

机译:LncRNA SLCO4A1-AS1通过增强miR-508-3p / PARD3轴的自噬作用来促进结直肠癌细胞增殖

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摘要

Aberrant expressions of various long non-coding RNAs (lncRNAs) have been involved in the progression and pathogenesis of various carcinomas. However, the expression and biological function of SLCO4A1-AS1 in colorectal cancer (CRC) remain poorly understood. Gain- and loss-of-function assays were applied to determine the roles of SLCO4A1-AS1 in autophagy and CRC progression. qRT-PCR and in situ hybridization (ISH) results showed that SLCO4A1-AS1 was positively associated with PARD3 expression in CRC tissues. In vitro and in vivo studies revealed that SLCO4A1-AS1 knockdown repressed cytoprotective autophagy as assayed by transmission electron microscopy (TEM), and inhibited cell proliferation by directly targeting partition-defective 3 (PARD3). Mechanistically, SLCO4A1-AS1 acted as a sponge of miR-508-3p, leading to upregulation of PARD3 and promotion of CRC cell proliferation. The current study demonstrates that the SLCO4A1-AS1/miR-508-3p/PARD3/autophagy pathway play a critical role in CRC cell proliferation, and might provide novel targets for developing therapeutic strategies for CRC.
机译:各种长非编码RNA(lncRNA)的异常表达已参与各种癌症的进展和发病机制。但是,SLCO4A1-AS1在结直肠癌(CRC)中的表达和生物学功能仍然知之甚少。功能获得和功能丧失测定用于确定SLCO4A1-AS1在自噬和CRC进展中的作用。 qRT-PCR和原位杂交(ISH)结果表明SLCO4A1-AS1与CRC组织中PARD3的表达呈正相关。体外和体内研究表明,如通过透射电子显微镜(TEM)检测到的,SLCO4A1-AS1敲低可抑制细胞保护性自噬,并通过直接靶向分区缺陷3(PARD3)抑制细胞增殖。从机制上讲,SLCO4A1-AS1充当miR-508-3p的海绵,导致PARD3上调并促进CRC细胞增殖。目前的研究表明,SLCO4A1-AS1 / miR-508-3p / PARD3 /自噬途径在CRC细胞增殖中起关键作用,并可能为开发CRC治疗策略提供新的靶点。

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