Department of Oncology, First Hospital of Shanxi Medical University, Taiyuan, Shanxi, China.
Cell Cycle. 2021 Jun;20(11):1080-1090. doi: 10.1080/15384101.2021.1924948. Epub 2021 May 16.
The long non-coding RNA HLA complex P5 (HCP5) is extensively related to cancer chemoresistance, while its function in gastric cancer (GC) has not been well elucidated yet. Here, the role and mechanism of HCP5 in regulating the chemoresistance of GC to cisplatin (DDP) was investigated. Our results revealed that HCP5 was increased in GC patients and indicated a poor prognosis. HCP5 knockdown weakens DDP resistance and reduced apoptosis of GC cells. miR-128 was decreased in GC patients and sponged by HCP5. HMGA2 was targeted by miR-128 and was increased in GC patients. HCP5 aggravated the resistance of GC cells to DDP in vitro by elevating HMGA2 expression via sponging miR-128. HCP5 silencing inhibited GC cells growth, resistance to DDP, and Ki-67 expression . In summary, HCP5 contributed to DDP resistance in GC cells through miR-128/HMGA2 axis, providing a promising therapeutic target for GC chemoresistance.
长链非编码 RNA HLA 复合物 P5（HCP5）与癌症化疗耐药性广泛相关，但其在胃癌（GC）中的作用尚未得到充分阐明。本研究旨在探讨 HCP5 在调节 GC 顺铂（DDP）化疗耐药性中的作用及其机制。研究结果表明，HCP5 在 GC 患者中上调，并提示预后不良。HCP5 敲低可减弱 DDP 耐药性并减少 GC 细胞凋亡。miR-128 在 GC 患者中下调，并被 HCP5 海绵吸附。HMGA2 是 miR-128 的靶基因，在 GC 患者中上调。HCP5 通过海绵吸附 miR-128 升高 HMGA2 表达，加重 GC 细胞对 DDP 的耐药性。HCP5 沉默抑制 GC 细胞生长、DDP 耐药性和 Ki-67 表达。综上所述，HCP5 通过 miR-128/HMGA2 轴促进 GC 细胞对 DDP 的耐药性，为 GC 化疗耐药性提供了有前景的治疗靶点。
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