周張杰　　藍(lán)燕麗　　藍(lán)翔　　蔡曉平

[關(guān)鍵詞] 肺癌;非小細(xì)胞肺癌;長(zhǎng)鏈非編碼RNA CA7-4;順鉑;耐藥;自噬

[中圖分類號(hào)] R329.2? ? ? ? ? [文獻(xiàn)標(biāo)識(shí)碼] A? ? ? ? ? [文章編號(hào)] 1673-9701（2021）20-0035-05

Long non-coding RNA CA7-4 in enhancing cisplatin resistance of lung cancer cell A594 by increasing autophagy levels

ZHOU Zhangjie1? ?LAN Yanli2? ?LAN Xiang2? ?CAI Xiaoping3

1.Department of General Medicine， Lishui Central Hospital in Zhejiang Province， Lishui? ?323000， China; 2.Department of Oncology， Lishui People′s Hospital in Zhejiang Province， Sixth Affiliated Hospital of Wenzhou Medical Univevsity， Lishui? ?323000， China; 3.Department of Respiratory Medicine， Lishui People′s Hospital in Zhejiang Province， Sixth Affiliated Hospital of Wenzhou Medical Univevsity， Lishui? ?323000， China

[Abstract] Objective To analyze the mechanism of long non-coding RNA （LncRNA） CA7-4 in affecting cisplatin （DDP） resistance in non-small cell lung cancer （NSCLC） cell line A549. Methods The human NSCLC cell line A549 was cultured in different concentrations of DDP， and the cell viability was measured to calculate the half maximal inhibitory concentration （IC50）. The A549 cells were divided into control group， DDP group， CA7-4 group and CA7-4+DDP group.The CA7-4 group and CA7-4+DDP group were transfected with CA7-4 pcDNA to up-regulate the level of LncRNA CA7-4. DDP group and CA7-4+DDP group were added with DDP at a final concentration of 12 μM. The cell viability， apoptosis rate and autophagy protein LC3Ⅰ and LC3Ⅱ levels of each group of cells were detected and compared. Results DDP can inhibit the growth of A549 cells in a dose-dependent manner. The IC50 value in this study was 12 μM. The level of LncRNA CA7-4 in the DDP group was significantly lower than that in the control group. The level of LncRNA CA7-4 in the CA7-4 group was significantly higher than that in the control group， and the LncRNA CA7-4 in the CA7-4+DDP group was significantly higher than that in the DDP group. The cell viability of the DDP group was significantly decreased and the apoptosis rate was significantly increased. The cell viability of the CA7-4 group was increased， and the apoptosis rate was decreased. The cell viability of the CA7-4+DDP group was significantly higher than that of the DDP group， while the apoptosis rate was significantly lower than that of the DDP group. The level of LC3Ⅱ/LC3Ⅰ in the DDP group was lower than that in the control group. The level of LC3Ⅱ/LC3Ⅰ in the CA7-4 group was higher than that in the control group. The level of LC3Ⅱ/LC3Ⅰ in the CA7-4+DDP group was significantly higher than that in the DDP group. Conclusion LncRNA CA7-4 can promote cell viability and inhibit cell apoptosis by promoting autophagy of NSCLC cell line A549， and promote cell resistance to DDP.