LncRNA MAGI2-AS3通过靶向调控miR-1269a/PTEN/AKT通路增强非小细胞肺癌对顺铂化疗的敏感性

doi:10.12122/j.issn.1673-4254.2024.10.22

南方医科大学学报 ›› 2024, Vol. 44 ›› Issue (10): 2033-2043.doi: 10.12122/j.issn.1673-4254.2024.10.22

• • 上一篇

LncRNA MAGI2-AS3通过靶向调控miR-1269a/PTEN/AKT通路增强非小细胞肺癌对顺铂化疗的敏感性

范喜瑞¹(), 戚之琳¹, 邓园洁², 杨子晗³, 孙丽⁴, 李国豪², 梁娟娟⁵, 吴菲³, 袁力文⁶

^1.皖南医学院，基础医学院生物化学与分子生物学教研室，安徽芜湖 241002
^2.皖南医学院，药学院，安徽芜湖 241002
^3.皖南医学院，临床医学院，安徽芜湖 241002
^4.皖南医学院，基础医学院生理学教研室，安徽芜湖 241002
^5.皖南医学院，检验学院，安徽芜湖 241002
^6.皖南医学院，麻醉学院，安徽芜湖 241002

收稿日期:2024-05-12 出版日期:2024-10-20 发布日期:2024-10-31
通讯作者: 范喜瑞 E-mail:20210006@wnmc.edu.cn
作者简介:范喜瑞，讲师，博士，E-mail: 20210006@wnmc.edu.cn
基金资助:
安徽省高校自然科学研究重点项目(2022AH051212);皖南医学院自然科学重点科研项目(WK2021Z16);大学生创新创业训练计划项目(202310368001)

LncRNA MAGI2-AS3 enhances cisplatin sensitivity of non-small cell lung cancer cells by regulating the miR-1269a/PTEN/AKT pathway

Xirui FAN¹(), Zhilin QI¹, Yuanjie DENG², Zihan YANG³, Li SUN⁴, Guohao LI², Juanjuan LIANG⁵, Fei WU³, Liwen YUAN⁶

^1.Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences,
^2.School of Pharmacy, Wannan Medical College, Wuhu 241002, China
^3.School of Clinical Medicine, Wannan Medical College, Wuhu 241002, China
^4.Department of Physiology, School of Basic Medical Sciences, Wannan Medical College, Wuhu 241002, China
^5.School of laboratory medicine, Wannan Medical College, Wuhu 241002, China
^6.School of Anesthesia, Wannan Medical College, Wuhu 241002, China

Received:2024-05-12 Online:2024-10-20 Published:2024-10-31
Contact: Xirui FAN E-mail:20210006@wnmc.edu.cn

摘要/Abstract

摘要：

目的研究lncRNA MAGI2-AS3对非小细胞肺癌顺铂耐药的影响及其分子机制。方法采用qRT-PCR 检测MAGI2-AS3和miR-1269a在顺铂敏感细胞（A549，H1299）和顺铂耐药细胞（A549/DDP，H1299/DDP）中的表达差异。采用慢病毒敲低A549和H1299中的MAGI2-AS3的表达，过表达A549/DDP和H1299/DDP中的MAGI2-AS3并加入20 μmol/L顺铂（DDP）处理。A549/DDP和H1299/DDP细胞实验分组为：OE-NC组，OE-MAGI2-AS3组，OE-NC+DDP组，OE-MAGI2-AS3+DDP组，A549和H1299细胞实验分组为：sh-NC组，sh-MAGI2-AS3组，sh-NC+DDP组，sh-MAGI2-AS3+DDP组。CCK-8和细胞克隆形成实验检测细胞存活率，流式细胞术和Western blotting分别检测细胞凋亡率和蛋白表达量，划痕实验和Transwell检测细胞EMT变化。通过网站GEPIA 、StarBase和miRDB预测MAGI2-AS3、miR-1269a和PTEN之间的靶向关系，并采用荧光素酶报告基因实验和RIP实验验证。采用miR-1269a mimic和pcDNA3.1-PTEN进行Rescue实验。结果 MAGI2-AS3在肺癌组织中的表达显著低于正常癌旁组织（P<0.05）且与患者不良预后相关（P<0.05）。A549/DDP和H1299/DDP中的MAGI2-AS3表达量显著低于A549和H1299（P<0.01）。干扰MAGI2-AS3可以显著促进顺铂处理前、后A549和H1299细胞的存活及EMT进程（P<0.01），同时降低顺铂诱导的细胞凋亡（P<0.005）。过表达MAGI2-AS3可以显著抑制顺铂处理前、后A549/DDP和H1299/DDP细胞存活与EMT进程（P<0.01），同时提升顺铂诱导的细胞凋亡（P<0.005）。MAGI2-AS3与miR-1269a结合在一起，miR-1269a与PTEN 3'UTR结合。在A549/DDP细胞内MAGI2-AS3通过靶向吸附miR-1269a促进PTEN的表达并下调AKT磷酸化从而抑制顺铂刺激下细胞的EMT进程（P<0.01）、促进顺铂诱导的A549/DDP细胞凋亡（P<0.01）。结论 LncRNA MAGI2-AS3通过靶向调控miR-1269a/PTEN/AKT信号轴增强非小细胞肺癌对顺铂化疗的敏感性。

关键词: LncRNA MAGI2-AS3, miR-1269a, 非小细胞肺癌, 顺铂耐药

Abstract:

Objective To investigate the mechanism mediating the regulatory effect of lncRNA MAGI2-AS3 on cisplatin (DDP) resistance in non-small cell lung cancer (NSCLC). Methods MAGI2-AS3 and miR-1269a expression levels were detected by qRT-PCR in DDP-sensitive lung cancer cell lines (A549 and H1299) and their resistant counterparts (A549/DDP and H1299/DDP). In A549 and H1299 cells with MAGI2-AS3 silencing and A549/DDP and H1299/DDP cells overexpressing MAGI2-AS3, the effects of 20 μmol/L DDP on cell viability and apoptosis were examined with CCK-8 assay, colony formation assay, flow cytometry and Western blotting, and the changes in epithelial-mesenchymal transition (EMT) were assessed with wound healing and Transwell assays. The interaction between MAGI2-AS3, miR-1269a and PTEN was predicted using GEPIA, StarBase and miRDB and verified with luciferase reporter gene assay and radioimmunoprecipitation (RIP) assay. A miR-1269a mimic and pcDNA3.1-PTEN plasmid were used to perform the rescue assay. Results MAGI2-AS3 expression was significantly downregulated in lung cancer tissues (P<0.05) in association with a poor prognosis (P<0.05). In the two DDP-resistant lung cancer cell lines, MAGI2-AS3 expression was significantly lowered as compared with the sensitive cells. Silencing MAGI2-AS3 significantly enhanced cell viability and promoted EMT of A549 and H1299 cells irrespective of DDP treatment, and also decreased DDP-induced apoptosis of the cells. In A549/DDP and H1299/DDP cells, MAGI2-AS3 overexpression strongly repressed cell viability and EMT irrespective of DDP treatment and promoted DDP-induced cell apoptosis. Luciferase reporter gene and RIP assays confirmed the binding of MAGI2-AS3 with miR-1269a and the binding of miR-1269a with 3 '-UTR domain of PTEN. The rescue assay demonstrated that MAGI2-AS3 acted as a sponge for miR-1269a to promote PTEN expression and downregulate AKT phosphorylation, thus inhibiting EMT and promoting DDP-induced apoptosis of A549/DDP cells. Conclusion MAGI2-AS3 enhances DDP sensitivity of NSCLC by targeted regulation of the miR-1269a/PTEN/AKT signaling axis.

Key words: long noncoding RNA MAGI2-AS3, miR-1269a, non-small cell lung cancer, cisplatin resistance

范喜瑞, 戚之琳, 邓园洁, 杨子晗, 孙丽, 李国豪, 梁娟娟, 吴菲, 袁力文. LncRNA MAGI2-AS3通过靶向调控miR-1269a/PTEN/AKT通路增强非小细胞肺癌对顺铂化疗的敏感性[J]. 南方医科大学学报, 2024, 44(10): 2033-2043.

Xirui FAN, Zhilin QI, Yuanjie DENG, Zihan YANG, Li SUN, Guohao LI, Juanjuan LIANG, Fei WU, Liwen YUAN. LncRNA MAGI2-AS3 enhances cisplatin sensitivity of non-small cell lung cancer cells by regulating the miR-1269a/PTEN/AKT pathway[J]. Journal of Southern Medical University, 2024, 44(10): 2033-2043.

图/表 6

表1 qRT-PCR所采用的引物序列

Tab.1 Primer sequence for qRT-PCR

Primer	Forward primers	Reverse primers
MAGI2-AS3	ACTGGAAATACAAGCCCAAGT	TTTCCACTCTGCTGGTTATGG
GAPDH	AGTCCACTGGCGTCTTCA	GAGTCCTTCCACGATACCAA
U6	TTATGGGTCCTAGCCTGAC	CACTATTGCGGGTCTGC
miR-1269a	GACTGAGCCGTGCTACTGG	TGTCGTGGAGTCGGCAATTG
PTEN	GTCAGAGGCGCTATGTGTATTA	TTAGCTGGCAGACCACAA

图1 LncRNA MAGI2-AS3在非小细胞肺癌顺铂耐药细胞系中低表达

Fig.1 Expression of MAGI2-AS3 in cisplatin-resistant NSCLC cell lines. A: qRT-PCR of MAGI2-AS3 in NSCLC cell lines A549, H1299, and HCC827 and in normal human lung epithelial cells (BEAS-2B). B: MAGI2-AS3 expression levels in LUAD tissues and normal adjacent tissues from the GEPIA database. C: Survival analysis of LUAD patients with high and low MAGI2-AS3 expressions. D, E: qRT-PCR of MAGI2-AS3 in cisplatin-sensitive A549 and H1299 cells and cisplatin-resistant A549/DDP and H1299/DDP cells. *P<0.05, **P<0.01, ***P<0.001.

图2 LncRNA MAGI2-AS3增强非小细胞肺癌对顺铂化疗的敏感性

Fig.2 MAGI2-AS3 overexpression enhances cisplatin sensitivity of non-small cell lung cancer cells. A, B, E, F: MAGI2-AS3 expressions in A549/DDP, A549, H1299/DDP and H1299 cells detected by qRT-PCR (**P<0.01, ***P<0.005 vs NC group). C, D, G, H: Viability of A549/DDP, A549, H1299/DDP and H1299 cells detected by CCK8 assay (#P<0.05, ###P<0.001 vs OE-NC group; &&&P<0.001 vs sh-NC group; **P<0.01, ***P<0.001). I, J: Viability of A549/DDP and A549 cells assessed by clone formation assay (#P<0.05 vs OE-NC group; &&&P<0.005 vs sh-NC group; **P<0.01, ***P<0.001). K, L: Apoptosis rates of A549/DDP, A549, H1299/DDP and H1299 cells detected by flow cytometry (###P<0.001 vs OE-NC group; &&&P<0.001 vs sh-NC group; **P<0.01, ***P<0.001). M-P: Western blotting for detecting Bax, Bcl-2, cleaved caspase3 protein expressions (**P<0.01, ***P<0.001 vs OE-NC group; ##P<0.01, ###P<0.001).

图3 LncRNA MAGI2-AS3抑制非小细胞肺癌EMT进程

Fig.3 MAGI2-AS3 overexpression inhibits EMT progression of NSCLC cells. A-D: Migration ability of A549, A549/DDP, H1299, and H1299/DDP cells assessed by wound healing assay (Scale bar=100 μm). E-H: Quantitation of the results of wound healing assay (**P<0.01, ***P<0.001 vs NC group; ##P<0.01, ###P<0.001). I, J: Invasion ability of A549 and A549/DDP assessed by Transwell assay (Scale bar=100 μm; *P<0.05, **P<0.01, ***P<0.001 vs NC group; ##P<0.01). K-N: Western blotting for detecting N-cadherin, E-cadherin, and vimentin protein expressions (**P<0.01, ***P<0.001 vs OE-NC group; ###P<0.001).

图4 LncRNA MAGI2-AS3通过靶向吸附miR-1269a增强A549/DDP细胞对顺铂的敏感性

Fig.4 MAGI2-AS3 enhances cisplatin sensitivity of A549/DDP cells by targeted adsorption of miR-1269a. A: qRT-PCR of MAGI2-AS3 expression in the nuclear and cytoplasmic fractions of A549/DDP cells. B: Schematic diagram showing the predicted wild-type and mutated binding sites for miR-1269a in MAGI2-AS3. C: qRT-PCR of miR-1269a expression in A549 and A549/DDP cells (**P<0.01). D: qRT-PCR of miR-1269a expression in A549/DDP and A549 cells with MAGI2-AS3 overexpression or knockdown (**P<0.01 vs OE-NC group; ##P<0.01 vs sh-NC group). E, F: qRT-PCR of MAGI2-AS3 and miR-1269a in A549/DDP cells treated with anti-AGO2 antibody in RIP assay (***P<0.001 vs IgG group). G: qRT-PCR of miR-1269a expression in A549/DDP cells transfected with the control mimic (NC) or miR-1269a mimic (**P<0.01). H: Luciferase activity of the reporter construct containing the wild-type or miR-1269a binding site mutant of MAGI2-AS3 (**P<0.01 vs mimic NC). I: qRT-PCR of miR-1269a in A549/DDP cells (**P<0.01). J: Transwell assay for assessing invasion ability of A549/DDP cells (Scale bar=100 μm; **P<0.01). K: Apoptosis rate of A549/DDP cells detected by flow cytometry (**P<0.01).

图5 LncRNA MAGI2-AS3 通过靶向miR-1269a/PTEN/AKT 通路增强非小细胞肺癌对顺铂的敏感性

Fig.5 MAGI2-AS3 overexpression enhances cisplatin sensitivity of NSCLC cells by targeting the miR-1269a/PTEN/AKT pathway. A: Schematic diagram showing the predicted wild-type and mutated binding sites between PTEN mRNA sequence and miR-1269a sequence. B: Spearman correlation analysis of MAGI2-AS3 and PTEN expression levels in LUAD tissues.C: Luciferase activity of the reporter construct containing the wild-type or mutant 3′UTR sequence of PTEN (***P<0.001 vs mimic NC group). D, E: PTEN mRNA and protein expression levels in A549/DDP cells (***P<0.001). F: qRT-PCR for detecting PTEN mRNA expression (**P<0.01). G: Western blotting for detecting expression levels of PTEN, p-AKT, AKT, E-cadherin, N-cadherin, and cleaved caspase-3 in A549/DDP cells. H: Transwell assay for assessing A549/DDP cell invasion ability (Scale bar=100 μm; ***P<0.001). I: Apoptosis rate of A549/DDP cells detected by flow cytometry (**P<0.01, ***P<0.001).

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LncRNA MAGI2-AS3通过靶向调控miR-1269a/PTEN/AKT通路增强非小细胞肺癌对顺铂化疗的敏感性

LncRNA MAGI2-AS3 enhances cisplatin sensitivity of non-small cell lung cancer cells by regulating the miR-1269a/PTEN/AKT pathway

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