硒蛋白SELENOI通过PI3K/AKT/mTOR信号通路促进胃癌增殖、迁移和侵袭

doi:10.3969/j.issn.1674-8115.2026.08.003

上海交通大学学报（医学版） ›› 2026, Vol. 46 ›› Issue (8): 1015-1025.doi: 10.3969/j.issn.1674-8115.2026.08.003

• 论著 · 基础研究 • 上一篇

硒蛋白SELENOI通过PI3K/AKT/mTOR信号通路促进胃癌增殖、迁移和侵袭

王铭杰, 倪博, 夏翔(), 张子臻()

上海交通大学医学院附属仁济医院胃肠外科，上海 200127

收稿日期:2026-03-11 接受日期:2026-04-03 出版日期:2026-08-13 发布日期:2026-08-13
通讯作者: 夏翔，主治医师，博士；电子信箱：xiaxiang@renji.com
张子臻，主任医师，博士；电子信箱：zhangzizhen@renji.com。
作者简介:第一联系人：张子臻及夏翔负责确定研究选题和设计，指导论文写作并提出修改意见；倪博负责论文审核及修改；王铭杰负责文献查阅、数据分析及初稿撰写。所有作者均阅读并同意了最终稿件的提交。
基金资助:
国家自然科学基金(82103510);国家自然科学基金(82303428);国家自然科学基金(82473077);国家自然科学基金(82473065);癌基因与相关基因国家重点实验室科研项目（课题）(KF2205-93);上海市卫生健康委员会医学新技术研究与转化种子计划项目(2024ZZ2020);上海市科学技术委员会三维电子腹腔内窥镜（微创外科领域）应用示范项目(25SF1905600);中央高校基本科研业务费专项资金(YG2026ZD15);仁济医院临床研究中心横向课题(IIT-2023-0001)

Selenoprotein SELENOI promotes the proliferation, migration and invasion of gastric cancer through the PI3K/AKT/mTOR signaling pathway

Wang Mingjie, Ni Bo, Xia Xiang(), Zhang Zizhen()

Department of Gastrointestinal Surgery, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China

Received:2026-03-11 Accepted:2026-04-03 Online:2026-08-13 Published:2026-08-13
Contact: Xia Xiang, E-mail: xiaxiang@renji.com
Zhang Zizhen, E-mail: zhangzizhen@renji.com.
About author:First author contact:Zhang Zizhen and Xia Xiang were responsible for the study conception and design, supervised manuscript preparation, and provided revision suggestions. Ni Bo was responsible for manuscript review and revision. Wang Mingjie was responsible for literature review, data analysis, and manuscript drafting. All authors have read and approved the final version of the manuscript and agreed to its submission.
Supported by:
National Natural Science Foundation of China(82103510);Research Project of the State Key Laboratory of Oncogenes and Related Genes(KF2205-93);Medical New Technology Research and Translation Seed Program of the Shanghai Municipal Health Commission(2024ZZ2020);Application Demonstration Project of Three-Dimensional Electronic Laparoscope in Minimally Invasive Surgery of the Science and Technology Commission of Shanghai Municipality(25SF1905600);Fundamental Research Funds for the Central Universities(YG2026ZD15);Horizontal Research Project of the Clinical Research Center, Renji Hospital(IIT-2023-0001)

摘要/Abstract

摘要：

目的·探讨硒蛋白I（SELENOI，即乙醇胺磷酸转移酶1）对胃癌细胞增殖、迁移与侵袭的调控作用及其分子机制。方法·利用蛋白质印迹法（Western blotting）和实时荧光定量PCR（quantitative real-time PCR，qPCR）检测SELENOI在胃黏膜上皮细胞及胃癌细胞系中的表达水平；收集2010—2015年上海交通大学医学院附属仁济医院胃肠外科100例胃腺癌患者的临床病理资料，分析SELENOI表达水平与患者预后的关联；基于癌症基因组图谱（The Cancer Genome Atlas，TCGA）数据库分析SELENOI在胃腺癌肿瘤组织和正常组织中的表达。筛选SELENOI高、低表达组间的差异基因，并进行京都基因与基因组百科全书（Kyoto Encyclopedia of Genes and Genomes，KEGG）通路富集分析，筛选SELENOI相关信号通路，同时通过qPCR和蛋白质印迹法验证SELENOI与该通路的调控关联；分别采用靶向SELENOI的小干扰RNA（small interfering RNA，siRNA）、SELENOI过表达质粒单独或联合哺乳动物雷帕霉素靶蛋白（mechanistic target of rapamycin，mTOR）抑制剂雷帕霉素处理HGC-27、NUGC-3胃癌细胞，通过细胞计数试剂盒-8（CCK-8）实验检测细胞增殖能力，Transwell实验检测细胞迁移、侵袭能力。结果·生物信息学分析发现SELENOI在胃癌组织中显著高表达（P<0.05）；100例胃腺癌患者Kaplan-Meier生存分析显示，SELENOI高表达患者预后更差（P=0.022）；qPCR和蛋白质印迹法结果证实，SELENOI在HGC-27、NUGC-3、AGS、MKN45胃癌细胞系中的表达水平显著高于胃黏膜上皮细胞GES-1（均P<0.05）；KEGG通路富集分析以及后续分子验证实验证实，胃癌中SELENOI可促进磷脂酰肌醇3-激酶（phosphatidylinositol 3-kinase，PI3K）/蛋白激酶B（protein kinase B，AKT）/mTOR信号通路活化；CCK-8与Transwell实验结果表明，SELENOI可通过激活PI3K/AKT/mTOR信号通路增强胃癌细胞的增殖、迁移和侵袭能力，而雷帕霉素可显著逆转该促癌效应。结论·SELENOI在胃癌组织及胃癌细胞中呈高表达状态；SELENOI可通过激活PI3K/AKT/mTOR信号通路促进胃癌细胞增殖、迁移及侵袭。

关键词: 硒蛋白I, 磷脂酰肌醇3-激酶, 蛋白激酶B, 哺乳动物雷帕霉素靶蛋白, 胃癌

Abstract:

Objective ·To investigate the regulatory role of the selenoprotein SELENOI (ethanolamine phosphotransferase 1, EPT1) in the proliferation, migration and invasion of gastric cancer cells, as well as its molecular mechanism. Methods ·The expression levels of SELENOI in gastric mucosal epithelial cells and gastric cancer cell lines were detected using Western blotting and quantitative real-time PCR (qPCR). The clinical pathological data of 100 patients who underwent surgery at the Department of Gastrointestinal Surgery of Renji Hospital, Shanghai Jiao Tong University School of Medicine, from 2010 to 2015 were collected, and the association between SELENOI expression levels and patient prognosis was analyzed. The expression of SELENOI in gastric adenocarcinoma tumor tissues and normal tissues was analyzed based on The Cancer Genome Atlas (TCGA) database. The differentially expressed genes between the SELENOI high- and low-expression groups were screened, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis was performed to select SELENOI-related signaling pathways. The regulatory association of SELENOI with this pathway was verified by qPCR and Western blotting. HGC-27 and NUGC-3 gastric cancer cells were treated with SELENOI-targeted small interfering RNA (siRNA), SELENOI overexpression plasmid alone, or in combination with the mechanistic target of rapamycin (mTOR) inhibitor rapamycin. The cell proliferation ability was detected by CCK-8 assay, and cell migration and invasion abilities were detected by Transwell assay. Results ·Bioinformatics analysis revealed that SELENOI was significantly highly expressed in gastric cancer tissues (P<0.05). Kaplan-Meier survival analysis of 100 patients with gastric adenocarcinoma showed that patients with high SELENOI expression had worse prognosis (P=0.022). qPCR and Western blotting results confirmed that the expression levels of SELENOI in HGC-27, NUGC-3, AGS, and MKN45 gastric cancer cell lines were significantly higher than those in gastric mucosal epithelial cells GES-1 (all P<0.05). KEGG pathway enrichment analysis and subsequent molecular validation experiments confirmed that SELENOI promoted the activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mTOR signaling pathway in gastric cancer. CCK-8 and Transwell assay results showed that SELENOI enhanced the proliferation, migration and invasion abilities of gastric cancer cells by activating the PI3K/AKT/mTOR signaling pathway, and rapamycin significantly reversed this tumor-promoting effect. Conclusion ·SELENOI is highly expressed in gastric cancer tissues and cells. SELENOI can promote the proliferation, migration and invasion of gastric cancer cells by activating the PI3K/AKT/mTOR signaling pathway.

Key words: SELENOI, phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT), mechanistic target of rapamycin (mTOR), gastric cancer

中图分类号:

R735.2

王铭杰, 倪博, 夏翔, 张子臻. 硒蛋白SELENOI通过PI3K/AKT/mTOR信号通路促进胃癌增殖、迁移和侵袭[J]. 上海交通大学学报（医学版）, 2026, 46(8): 1015-1025.

Wang Mingjie, Ni Bo, Xia Xiang, Zhang Zizhen. Selenoprotein SELENOI promotes the proliferation, migration and invasion of gastric cancer through the PI3K/AKT/mTOR signaling pathway[J]. Journal of Shanghai Jiao Tong University (Medical Science), 2026,(8): 1015-1025.

图/表 9

表1 siRNA序列

Tab 1 Sequences of siRNA

Name	Forward (5'→3')	Reverse (5'→3')
siRNA-NC	UUCUCCGAACGAGUCACGUTT	ACGUGACUCGUUCGGAGAATT
siRNA-SELENOI-1	CCUAGAGUAUUCUACUUUATT	UAAAGUAGAAUACUCUAGGTT
siRNA-SELENOI-2	GAUUAUUGGUUGUGCAUUATT	UAAUGCACAACCAAUAAUCTT
siRNA-SELENOI-3	GGAUAGUUGGUCAUGUGUUTT	AACACAUGACCAACUAUCCTT

表2 qPCR引物序列

Tab 2 Primer sequences for qPCR

Gene	Forward (5'→3')	Reverse (5'→3')
GAPDH	GAGAAGGCTGGGGCTCATTT	AGTGATGGCATGGACTGTGG
SELENOI	AAGCAAGCTCGCAGAACCAA	ATGTCATATCCCCATGGCAGG
PI3K	CTTTGGCCAGTACCTCATGGA	TGTTACTCAGTCCTGCGTGG
AKT	CTCTTTCCAGACCCACGACC	TAATGTGCCCGTCCTTGTCC
mTOR	GATGACTGGCTGGAATGGCT	GGTCTGTGTGACTTCAGCGA

图1 SELENOI在胃癌中的表达水平Note： A. Upregulated expression of SELENOI in tumor tissues compared with normal tissues in the TCGA-STAD cohort. B/C. Elevated SELENOI expression levels in gastric cancer cell lines (HGC-27, NUGC-3, AGS, and MKN45) compared with GES-1 normal gastric epithelial cells, measured by qPCR (B) and Western blotting (C), respectively. ①P=0.004, ②P<0.001.

Fig 1 Expression levels of SELENOI in gastric cancer

图2 SELENOI表达与STAD临床特征的相关性分析Note： A‒C. Immunohistochemical staining of SELENOI protein in 100 STAD tissue specimens. Representative immunohistochemical images of stage Ⅰ (A, IRS=0), stage Ⅱ (B, IRS=4), and stage Ⅲ (C, IRS=8) STAD tissues. D. Immunohistochemical quantification of SELENOI protein expression in 100 STAD tissues, classification of patients into SELENOI-high and SELENOI-low expression groups, and Kaplan-Meier survival analysis of the association between SELENOI expression and patient survival.

Fig 2 Correlation analysis of SELENOI expression and clinical characteristics of STAD

表3 STAD患者不同SELENOI表达组临床病理特征的比较

Tab 3 Comparison of clinicopathological characteristics between patients with high and low SELENOI expression

Characteristic	SELENOI high-expression group (n=50)	SELENOI low-expression group (n=50)	t/Z/χ² value	P value
Age/year	64.80±10.97	62.62±12.34	0.934	0.386
Gender/n(%)			0.049	0.826
Male	35 (70.0)	36 (72.0)
Female	15 (30.0)	14 (28.0)
T stage/n(%)			0.798	0.425
T1	1 (2.0)	1 (2.0)
T2	1 (2.0)	3 (6.0)
T3	6 (12.0)	7 (14.0)
T4	42 (84.0)	39 (78.0)
N stage/n(%)			0.279	0.780
N0	10 (20.0)	12 (24.0)
N1	10 (20.0)	7 (14.0)
N2	12 (24.0)	15 (30.0)
N3	18 (36.0)	16 (32.0)
Clinical stage/n(%)			0.713	0.476
Ⅰ	0 (0)	1 (2.0)
Ⅱ	13 (26.0)	15 (30.0)
Ⅲ	37 (74.0)	34 (68.0)
Ⅳ	0 (0)	0 (0)

图3 SELENOI 表达相关差异基因的KEGG通路富集分析Note： A. Volcano plot showing differentially expressed genes (TCGA-STAD cohort). B. KEGG pathway enrichment analysis of SELENOI-associated differentially expressed genes (TCGA-STAD cohort).

Fig 3 KEGG pathway enrichment analysis of SELENOI-associated differentially expressed genes in TCGA-STAD

图4 沉默及过表达 SELENOI 对胃癌细胞增殖、迁移及侵袭能力的影响Note： A. Assessment of SELENOI knockdown efficiency after si-SELENOI transfection by qPCR and Western blotting. B. Confirmation of SELENOI overexpression plasmid efficiency by qPCR and Western blotting. C. Impact of si-SELENOI on the proliferation of gastric cancer cell lines by CCK-8 assay. Statistical comparisons were made with the si-NC group. D. Impact of si-SELENOI on the migration and invasion capacities of gastric cancer cell lines determined by Transwell assay. ①P<0.001, ②P=0.025.

Fig 4 Effect of SELENOI silencing and overexpression on the proliferation, migration, and invasion abilities of gastric cancer cells

图5 SELENOI对PI3K/AKT/mTOR信号通路的调控Note： A. Effects of si-SELENOI on the expression of the PI3K/AKT/mTOR pathway components detected byqPCR and Western blotting. B. Effects of SELENOI overexpression on the expression of the PI3K/AKT/mTOR pathway components determined by qPCR and Western blotting. ①P=0.349, ②P>0.999, ③P=0.772, compared with the si-NC group; ④P=0.468, ⑤P=0.100, ⑥P=0.106, compared with the vector group.

Fig 5 Regulation of the PI3K/AKT/mTOR signaling pathway by SELENOI

图6 SELENOI通过调控PI3K/AKT/mTOR通路促进胃癌细胞增殖、迁移和侵袭Note： A. Western blotting analysis of PI3K/AKT/mTOR signaling pathway components in SELENOI overexpression HGC-27 gastric cancer cells treated with rapamycin. B. CCK-8 assay assessing the proliferation of HGC-27 gastric cancer cells overexpressing SELENOI and incubated with rapamycin. C/D. Transwell assays examining the migration (C) and invasion (D) capacities of rapamycin-treated HGC-27 gastric cancer cells with SELENOI overexpression. ①P=0.029, ②P=0.015, ③P=0.008, ④P<0.001.

Fig 6 SELENOI promotes the proliferation, migration and invasion of gastric cancer cells through regulation of the PI3K/AKT/mTOR pathway

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硒蛋白SELENOI通过PI3K/AKT/mTOR信号通路促进胃癌增殖、迁移和侵袭

Selenoprotein SELENOI promotes the proliferation, migration and invasion of gastric cancer through the PI3K/AKT/mTOR signaling pathway

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