红景天苷靶向miR-1343-3p-OGDHL/PDHB糖代谢轴抑制胃癌细胞的体内外增殖

doi:10.12122/j.issn.1673-4254.2025.06.12

南方医科大学学报 ›› 2025, Vol. 45 ›› Issue (6): 1226-1239.doi: 10.12122/j.issn.1673-4254.2025.06.12

红景天苷靶向miR-1343-3p-OGDHL/PDHB糖代谢轴抑制胃癌细胞的体内外增殖

侯鑫睿¹^,²(), 张振东¹^,², 曹明远¹^,², 杜予心¹^,², 王小平¹()

^1.西藏民族大学，医学院，陕西咸阳 712082
^2.西藏民族大学，高海拔缺氧环境与生命健康重点实验室，陕西咸阳 712082

收稿日期:2025-03-21 出版日期:2025-06-20 发布日期:2025-06-27
通讯作者: 王小平 E-mail:362380328@qq.com;xpwang@xzmz.edu.cn
作者简介:侯鑫睿，在读硕士研究生，E-mail: 362380328@qq.com
基金资助:
国家自然科学基金(82460515);陕西省自然科学基础研究计划项目(2025JC-YBMS-1088);中央引导地方科技发展资金项目(LSKJ202447);咸阳市科技计划重点研发项目(L2024-ZDYF-SF-0025);西藏民族大学研究生科研创新与实践项目(Y2025140)

Salidroside inhibits proliferation of gastric cancer cells by regulating the miR-1343-3p-OGDHL/PDHB glucose metabolic axis

Xinrui HOU¹^,²(), Zhendong ZHANG¹^,², Mingyuan CAO¹^,², Yuxin DU¹^,², Xiaoping WANG¹()

^1.School of Medicine, Xizang Minzu University, Xianyang 712082, China
^2.Key Laboratory of High Altitude Hypoxia Environment and Life Health, Xizang Minzu University, Xianyang 712082, China

Received:2025-03-21 Online:2025-06-20 Published:2025-06-27
Contact: Xiaoping WANG E-mail:362380328@qq.com;xpwang@xzmz.edu.cn
Supported by:
National Natural Science Foundation of China(82460515)

摘要/Abstract

摘要：

目的探讨红景天苷抗胃肿瘤（GC）机制，强调糖代谢重编程途径。方法高通量测序结合生物信息学分析预测红景天苷作用后显著差异表达的miRNA-靶mRNA，mRNA-mRNA相互作用关系，RNA结合蛋白免疫共沉淀实验验证miRNA-mRNA互作，蛋白质免疫共沉淀（Co-IP）实验验证下游靶mRNA-mRNA互作。通过体外及体内实验探究红景天苷与miR-1343-3p对GC的作用机制。体外实验通过CCK-8法确定红景天苷的IC₅₀值并分低、中、高剂量处理细胞，结合克隆实验、RT-qPCR、Western blotting、ELISA及ATP检测评估药物对增殖、基因/蛋白/下游分子表达（miRNA、mRNA、丙酮酸、乙酰CoA）及能量代谢的影响；进一步以脂质体法转染miR-1343-3p模拟物（miR-1343-3p mimic）、抑制剂（miR-1343-3p inhibitor）、靶向OGDHL的siRNA（si-OGDHL）及其阴性对照（NC mimic/NC inhibitor/si-NC）至GC细胞，联合红景天苷处理，通过相同方法验证其协同作用。体内实验通过构建荷瘤裸鼠模型，给予红景天苷和miR-1343-3p激动剂（miR-1343-3p agomir）干预，分析瘤块体积/质量变化及靶基因、蛋白表达与代谢状态。实验分组包括空白对照、单药组及联合组，系统解析红景天苷与miRNA的调控网络。结果生物信息学证实，miR-1343-3p与三羧酸（TCA）循环关键酶α-酮戊二酸脱氢酶复合体亚基（OGDHL）呈负相关（P<0.01），且直接相互作用。OGDHL与丙酮酸脱氢酶E1亚基-β（PDHB）在胃癌组织中同步高表达，且二者存在相互作用。体外与体内实验证实，红景天苷以剂量/时间依赖性抑制GC细胞增殖，红景天苷作用GC细胞后，重要抑癌因子miR-1343-3p升高，受其调控的OGDHL的基因表达明显下调，导致与之互作的糖酵解酶蛋白PDHB稳态失衡，丙酮酸氧化脱羧减少，产物乙酰CoA和ATP生成明显减少（P<0.05）。结论红景天苷可能通过调控miR-1343-3p-OGDHL/PDHB酶复合体-丙酮酸糖代谢通路抑制GC细胞的增殖，为红景天苷抗肿瘤机制提供了新的见解，为开发基于代谢酶复合体协同调控癌症的精准疗法提供理论依据。

关键词: 胃癌, 糖代谢重编程, 红景天苷, miR-1343-3p, OGDHL, PDHB

Abstract:

Objective To investigate the mechanism through which salidroside inhibits proliferation of gastric cancer (GC) cells focusing on glucose metabolic reprogramming pathways. Methods High-throughput sequencing combined with bioinformatics analysis was employed to identify the potential targets of salidroside in human GC MGC-803 cells. Liposome-mediated transfection experiments were carried out to validate the functional and mechanistic roles of these targets. CCK-8 and colony formation assays were used to assess the effects of salidroside on GC cell viability and clonogenic ability. qRT-PCR, Western blotting, and biochemical assay kits were used to analyze the regulatory effects of salidroside on the miR-1343-3p-OGDHL/PDHB enzyme complex-pyruvate metabolic pathway in GC cells. Results Bioinformatics analysis suggested that the tumor-suppressive factor miR-1343-3p negatively regulated the key glycolytic enzyme gene oxoglutarate dehydrogenase-like (OGDHL) in GC cells, and OGDHL and pyruvate dehydrogenase E1 subunit beta (PDHB) were both significantly upregulated in GC tissues, which was close by correlated with reduced survival rates of GC patients. In MGC-803 cells, salidroside treatment significantly enhanced the expression level of miR-1343-3p and downregulated OGDHL expression, resulting in disruption of the stability of PDHB, reduced pyruvate oxidative decarboxylation, and consequently decreased production of acetyl-CoA and ATP. Conclusion Salidroside inhibits GC cell proliferation possibly by regulating the miR-1343-3p-OGDHL/PDHB enzyme complex-pyruvate metabolic pathway, which provides new insights into its anti-tumor mechanisms and suggests new strategies for targeted therapy for GC.

Key words: gastric cancer, glucose metabolic reprogramming, salidroside, miR-1343-3p, oxoglutarate dehydrogenase-like, pyruvate dehydrogenase E1 subunit beta

侯鑫睿, 张振东, 曹明远, 杜予心, 王小平. 红景天苷靶向miR-1343-3p-OGDHL/PDHB糖代谢轴抑制胃癌细胞的体内外增殖[J]. 南方医科大学学报, 2025, 45(6): 1226-1239.

Xinrui HOU, Zhendong ZHANG, Mingyuan CAO, Yuxin DU, Xiaoping WANG. Salidroside inhibits proliferation of gastric cancer cells by regulating the miR-1343-3p-OGDHL/PDHB glucose metabolic axis[J]. Journal of Southern Medical University, 2025, 45(6): 1226-1239.

图/表 13

表1 引物和寡核苷酸序列

Tab.1 Primer and oligonucleotide sequences

Primer name	Direction	Sequence (5'→3')
GAPDH	Forward	TGACATCAAGAAGGTGGTGAAGCAG
GAPDH	Reverse	GTGTCGCTGTTGAAGTCAGAGGAG
U6	Forward	GCTTCGGCAGCACATATACTAAAAT
U6	Reverse	CGCTTCACGAATTTGCGTGTCAT
miR-1343-3p	Forward	CGCGGCCTTAATGCTAATTGTGA
miR-1343-3p	Reverse	AGTGCAGGGTCCGAGGTATT
OGDHL	Forward	ATCACTCTGTCGCTGGTTGCC
OGDHL	Reverse	CGCTCAGGTGGAAGGTCTCATATAC
PDHB	Forward	TTCTCCATGCAAGCCATTGACCAG
PDHB	Reverse	CTACACCTGCTGAGGCACCATTG
miR-1343-3p mimic	Sense	CUCCUGGGGCCCGCACUCUCGCUU
miR-1343-3p mimic	Antisense	AAGCGAGAGUGCGGGCCCAGGAG
NC mimic	Sense	UCACAACCUCCUAGAAAGAGUAGA
NC mimic	Antisense	UCUACUCUUUCUAGGAGGUUGUGA
miR-1343-3p inhibitor	Antisense	AAGCGAGAGUGCGGGCCCCAGGAG
NC inhibitor	Antisense	UCUACUCUUUCUAGGAGGUUGUGA
miR1343-3p agomir	sense	CUCCUGGGGCCCGCACUCUCGCUU
miR1343-3p agomir	antisense	AAGCGAGAGUGCGGGCCCAGGAG
si-OGDHL	Sense	CCCUCAGACUUGAUCACAAdTdT
si-OGDHL	Antisense	UUGUGAUCAAGUCUGAGGGdTdT
si-NC	Sense	UUCUCCGAACGUGUCACGUdTdT
si-NC	Antisense	ACGUGACACGUUCGGAGAAdTdT

图1 高通量测序结合生物信息学分析miR-1343-3p与OGDHL相互作用关系

Fig.1 High-throughput sequencing combined with bioinformatics analysis for interaction between miR-1343-3p and OGDHL. A: Changes in miR-1343-3p and OGDHL in human gastric cancer cells after salidroside treatment detected by high-throughput sequencing. B: miRNA network and target gene analysis of the interaction between OGDHL and miR-1343-3p. C: Pearson correlation and genomic locus analysis of the association of OGDHL with miR-1343-3p in human gastric cancer cells. D: RNA immunoprecipitation assay for validating the interaction between OGDHL and miR-1343-3p. **P<0.01 vs Control/Ig G group (n=3).

图2 OGDHL与PDHB蛋白的相互作用关系

Fig.2 Interaction between OGDHL and PDHB proteins. A: Bioinformatics analysis of the OGDHL-PDHB interaction network. B: Co-immunoprecipitation assay for confirming their binding (**P<0.01, ***P<0.001 vs Input; n=3). C: Differential expression of OGDHL and PDHB in gastric cancer (GC) tissues from The Cancer Genome Atlas (TCGA) (**P<0.01 vs Normal; n=3). D: Gene Expression Profiling Interactive Analysis (GEPIA) showing a negative correlation between high OGDHL/PDHB expression and clinical outcomes of GC patients, highlighting a significantly shorter overall survival (OS) of patients in high-expression groups.

图3 红景天苷通过miR-1343-3p-OGDHL/PDHB轴抑制胃癌细胞的增殖

Fig.3 Salidroside inhibits proliferation of gastric cancer cells through the miR-1343-3p-OGDHL/PDHB axis. A: CCK-8 assay for assessing viability of MGC-803 cells treated with different concentrations of salidroside for 24 h/48 h. B: Colony formation assay of GC cells after salidroside treatment. C: qRT-PCR analysis showing changes in miR-1343-3p, OGDHL, and PDHB in GC cells after salidroside treatment. *P<0.05, **P<0.01, ***P<0.001 vs 0 μmol/mL or NS model (n=3).

图4 红景天苷作用后观察下游蛋白分子能量的表达

Fig.4 Expression of downstream protein molecules and energy-related metabolites post-salidroside treatment. A: Western blotting results. B: Detection results of pyruvate, acetyl-CoA, and ATP in salidroside-treated GC cells using biochemical assay kits. *P<0.05, **P<0.01, ***P<0.001 vs NS model (n=3).

图5 miR-1343-3p mimic与miR-1343-3p inhibitor在细胞中的转染效率及细胞的功能性变化

Fig.5 Transfection efficiency and functional changes of miR-1343-3p mimic/inhibitor in human GC cells. A: Successful transfection of miR-1343-3p mimic or inhibitor into human GC cells (***P<0.01 vs NC mimic, **P<0.001 vs NC inhibitor; n=3). B-E: Effects of miR-1343-3p mimic/inhibitor on cell viability and clonogenic ability of GC cells (*P<0.05, **P<0.01, ***P<0.01 vs Control; ###P<0.001 vs Salidroside; n=3).

图6 miR-1343-3p mimic协同红景天苷调控胃癌细胞的生长

Fig.6 Synergistic regulation of GC cell growth by miR-1343-3p mimics and salidroside. A-C: Results of qRT-PCR, Western blotting, and biochemical assays for assessing changes in miR-1343-3p, OGDHL, PDHB, pyruvate, acetyl-CoA, and ATP levels in GC cells treated with miR-1343-3p mimic or inhibitors. *P<0.05, ***P<0.001 vs Control; ###P<0.001 vs NC mimic (n=3).

图7 miR-1343-3p inhibitor逆转了红景天苷调控胃癌细胞生长的抑制作用

Fig.7 miR-1343-3p inhibitor reverses salidroside-mediated suppression of GC cell growth. A-C: Results of qRT-PCR, Western blotting, and biochemical detection miR-1343-3p, OGDHL, PDHB, pyruvate, acetyl-CoA, and ATP levels in GC cells following miR-1343-3p inhibitor treatment. **P<0.01, ***P<0.001 vs Control, ##P<0.01, ###P<0.001 vs Salidroside; †††P<0.001 vs NC inhibitor, ‡‡‡P<0.001 vs Salidroside+NC inhibitor; C: ###P<0.001 vs miR-1343-3p inhibitor (n=3).

图8 si-OGDHL在细胞中的转染效率及形态学变化

Fig.8 Transfection efficiency and functional changes of si-OGDHL in human GC cells. A: Successful transfection of si-OGDHL into GC cells. B, C: Effects of si-OGDHL on cell viability and clonogenic ability in GC cells. *P<0.05, ***P<0.001 vs Control (n=3).

图9 敲低OGDHL协同红景天苷抑制胃癌细胞生长

Fig.9 Knockdown of OGDHL synergizes with salidroside to inhibit GC cell growth. A-C: Results of qRT-PCR, Western blotting, and assay kits for miR-1343-3p, OGDHL, PDHB, pyruvate, acetyl-CoA, and ATP levels in GC cells treated with si-OGDHL. *P<0.05, ***P<0.001 vs Control; ###P<0.001 vs Salidroside; †P<0.05, †††P<0.001 vs si-NC, ‡‡‡P<0.001 vs Salidroside+si-NC (n=3).

图10 不同方法处理组作用后,胃癌细胞中miR-1343-3p, OGDHL, PDHB及丙酮酸、乙酰CoA和ATP水平的变化

Fig.10 Changes in miR-1343-3p, OGDHL, PDHB, pyruvate, acetyl-CoA, and ATP levels in GC cells following different treatments. A-C:Results of qRT-PCR, Western blotting and biochemical assay kits for detecting miR-1343-3p, OGDHL, PDHB, pyruvate, acetyl-CoA and ATP levels in GC cells treated with salidroside, miR-1343-3p mimic, miR-1343-3p inhibitor and si-OGDHL. *P<0.05, **P<0.01, ***P<0.001 vs Control (n=3).

图11 异种移植GC细胞后观察活体内瘤块形态变化

Fig.11 Observation of morphological changes in tumor masses after xenografting of GC cells in nude mice. A-C: Gross appearance and comparison of volume/weight in tumor masses treated with salidroside and miR-1343-3p overexpression. **P<0.01, ***P<0.001 vs Control.

图12 红景天苷同miR-1343-3p在活体内抑制胃癌肿瘤生长

Fig.12 Salidroside and miR-1343-3p inhibit gastric cancer tumor growth in nude mice. A-C: Changes in miR-1343-3p levels, OGDHL and PDHB expression, and concentrations of pyruvate, acetyl-CoA, and ATP in tumor tissues analyzed by qRT-PCR, Western blotty, and biochemical kits. *P<0.05, **P<0.01, ***P<0.001 vs Control.

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红景天苷靶向miR-1343-3p-OGDHL/PDHB糖代谢轴抑制胃癌细胞的体内外增殖

Salidroside inhibits proliferation of gastric cancer cells by regulating the miR-1343-3p-OGDHL/PDHB glucose metabolic axis

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