The introduction of long non-coding RNAs (lncRNAs) has revolutionized the treatment of hepatocellular carcinoma (HCC). Thus, in the present study, we aimed to evaluate the effect of a newly found lncRNA, LINC00160, on autophagy and drug resistance of HCC. Interaction among LINC00160, miR-132 and PIK3R3 was verified by dual luciferase reporter gene assay. Loss- and gain-of function experiments were conducted in HCC cells to explore the roles of LINC00160, miR-132 and PIK3R3 in HCC by determining cell viability, autophagy and apoptosis. Finally, tumorigenicity in nude mice was established to confirm the in vitro findings. LINC00160 and PIK3R3 were up-regulated but miR-132 was down-regulated in HCC tissues and cells. LINC00160 may regulate miR-132 and PIK3R3 was the target gene of miR-132. LINC00160 increased the expression of LC3I/LC3II and Atg5 but decreased the p62 expression, while silencing of LINC00160 or over-expression of miR-132 suppressed HCC cell viability, autophagy, drug-resistance and tumorigenicity in nude mice but promoted HCC cell apoptosis by inhibiting the PIK3R3 expression. Taken together, silencing of LINC00160 suppresses autophagy and drug resistance in HCC by regulating miR-132-targeted PIK3R3.

中文翻译：

---

长链非编码 RNA LINC00160 作为 microRNA-132 的诱饵，通过抑制 PIK3R3 介导肝细胞癌的自噬和耐药性。

长链非编码 RNA (lncRNA) 的引入彻底改变了肝细胞癌 (HCC) 的治疗。因此，在本研究中，我们旨在评估新发现的 lncRNA LINC00160 对 HCC 自噬和耐药性的影响。LINC00160、miR-132 和 PIK3R3 之间的相互作用通过双荧光素酶报告基因检测得到验证。在 HCC 细胞中进行功能丧失和获得实验，通过确定细胞活力、自噬和凋亡来探索 LINC00160、miR-132 和 PIK3R3 在 HCC 中的作用。最后，建立了裸鼠的致瘤性以证实体外研究结果。LINC00160 和 PIK3R3 在 HCC 组织和细胞中上调，但 miR-132 下调。LINC00160可能调节miR-132，PIK3R3是miR-132的靶基因。LINC00160 增加了 LC3I/LC3II 和 Atg5 的表达，但降低了 p62 的表达，而 LINC00160 的沉默或 miR-132 的过表达抑制了裸鼠中 HCC 细胞的活力、自噬、耐药性和致瘤性，但通过抑制促进 HCC 细胞凋亡PIK3R3 表达。总之，LINC00160 的沉默通过调节 miR-132 靶向 PIK3R3 来抑制 HCC 中的自噬和耐药性。