LINC00511 通过与 miR-182-3p 和 BIRC5 相互作用抑制肺腺癌对顺铂的耐药性。
LINC00511 Knockdown Suppresses Resistance to Cisplatin in Lung Adenocarcinoma by Interacting with miR-182-3p and BIRC5.
机构信息
Department of Radiotherapy, Cangzhou Central Hospital, No. 16 Xinhua West Road, Cangzhou, 061000, Hebei, China.
Return Visit Office, Cangzhou Central Hospital, Cangzhou, 061000, Hebei, China.
出版信息
Mol Biotechnol. 2022 Mar;64(3):252-262. doi: 10.1007/s12033-021-00400-0. Epub 2021 Sep 30.
We studied the role of long intergenic non-protein coding RNA 00,511 (LINC00511) in lung adenocarcinoma (LUAD), with a specific focus on acquired chemoresistance. LINC00511 expression was higher in responders to cisplatin (DDP, another name for cisplantin) than non-responders, in A549/DDP cells than in parental A549 cells and normal human bronchial epithelial cells (16HBE). LINC00511 knockdown decreased the half maximal inhibitory concentration (IC50) value, suppressed A549/DDP cell viability, but induced apoptosis. LINC00511 bound with miR-182 and increased the expression of baculoviral inhibitor of apoptosis protein (IAP) repeat containing 5 (BIRC5). BIRC5 knockdown mimicked the effects of LINC00511 knockdown on the IC50 value, A549/DDP cell viability, and apoptosis. BIRC5 overexpression negated the effects of LINC00511 knockdown on A549/DDP cells. In vivo, LINC00511 knockdown attenuated the tumorigenesis of A549/DDP cells after DDP injection. These results provide a novel LINC00511/miR-182/BIRC5 paradigm to explain the mechanism of acquired DDP resistance.
我们研究了长链非编码 RNA 00511（LINC00511）在肺腺癌（LUAD）中的作用，特别是在获得性化疗耐药方面。与非应答者相比，应答顺铂（DDP，另一种名称为顺铂）的 A549/DDP 细胞中 LINC00511 的表达更高，而 A549 细胞和正常人类支气管上皮细胞（16HBE）中则较低。LINC00511 敲低降低了半最大抑制浓度（IC50）值，抑制了 A549/DDP 细胞的活力，但诱导了细胞凋亡。LINC00511 与 miR-182 结合，并增加了杆状病毒凋亡抑制蛋白（IAP）重复序列 5（BIRC5）的表达。BIRC5 敲低模拟了 LINC00511 敲低对 IC50 值、A549/DDP 细胞活力和细胞凋亡的影响。BIRC5 的过表达否定了 LINC00511 敲低对 A549/DDP 细胞的影响。在体内，DDP 注射后 LINC00511 敲低减弱了 A549/DDP 细胞的致瘤性。这些结果提供了一个新的 LINC00511/miR-182/BIRC5 范例，以解释获得性 DDP 耐药的机制。
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