Long noncoding RNA LINC00482 (LINC00482) is dysregulated in non-small cell lung cancer cells (NSCLC). Herein, this research examined the actions and specific mechanisms of LINC00482 in cisplatin (DDP) resistance in NSCLC. LINC00482 expression was assessed using RT-qPCR in clinical NSCLC tissues and cell lines. Knockdown and ectopic expression assays were conducted in A549 and HCC44 cells, followed by determination of cell proliferation with CCK-8 and clone formation assays, apoptosis with flow cytometry, and DDP sensitivity. The association between LINC00482, E2F1, and CLASRP was evaluated with dual-luciferase reporter, ChIP, and RIP assays. The role of LINC00482 in NSCLC was confirmed in nude mice. NSCLC tissues and cells had upregulated LINC00482 expression. LINC00482 was mainly localized in the cell nucleus, and LINC00482 recruited E2F1 to enhance CLASRP expression in NSCLC cells. LINC00482 knockdown enhanced the DDP sensitivity and apoptosis of NSCLC cells while reducing cell proliferation, which was negated by overexpressing CLASRP. LINC00482 knockdown restricted tumor growth and enhanced DDP sensitivity in NSCLC in vivo. LINC00482 silencing downregulated CLASRP through E2F1 to facilitate the sensitivity to DDP in NSCLC.

长非编码 RNA LINC00482 (LINC00482) 在非小细胞肺癌细胞 (NSCLC) 中失调。在此，本研究探讨了 LINC00482 在 NSCLC 顺铂 (DDP) 耐药中的作用和具体机制。使用 RT-qPCR 评估临床 NSCLC 组织和细胞系中的 LINC00482 表达。在 A549 和 HCC44 细胞中进行敲低和异位表达测定，然后使用 CCK-8 和克隆形成测定测定细胞增殖，使用流式细胞术测定细胞凋亡，以及 DDP 敏感性。通过双荧光素酶报告基因、ChIP 和 RIP 测定评估 LINC00482、E2F1 和 CLASRP 之间的关联。 LINC00482 在 NSCLC 中的作用在裸鼠中得到证实。 NSCLC 组织和细胞的 LINC00482 表达上调。 LINC00482主要定位于细胞核，LINC00482招募E2F1来增强NSCLC细胞中CLASRP的表达。 LINC00482 敲低增强了 NSCLC 细胞的 DDP 敏感性和凋亡，同时减少了细胞增殖，而过表达 CLASRP 则抵消了这一作用。 LINC00482 敲低限制了 NSCLC 体内肿瘤生长并增强了 DDP 敏感性。 LINC00482 通过 E2F1 沉默下调 CLASRP，以提高 NSCLC 对 DDP 的敏感性。