LINC01123通过结合ENO1促进胃癌的增殖和糖酵解

doi:10.3969/j.issn.1674-8115.2025.11.004

上海交通大学学报（医学版） ›› 2025, Vol. 45 ›› Issue (11): 1443-1457.doi: 10.3969/j.issn.1674-8115.2025.11.004

• 论著 · 基础研究 • 上一篇

LINC01123通过结合ENO1促进胃癌的增殖和糖酵解

张舒琼¹^,²^,³^,⁴, 柯星¹, 赵兴贺¹, 陈晓翠¹, 郑浩东¹, 陈惠¹, 沈立松¹^,²^,³(), 杨俊瑶¹^,³^,⁵()

^1.上海交通大学医学院附属新华医院检验科，上海 200092
^2.上海交通大学医学院医学技术学院医学检验技术系，上海 200025
^3.上海市实验医学研究院智慧医学研究所，上海 200092
^4.广东省深圳市第二人民医院检验科，深圳 518035
^5.上海交通大学医学院附属新华医院临床研究中心，上海 200092

收稿日期:2025-05-29 接受日期:2025-06-30 出版日期:2025-11-28 发布日期:2025-12-03
通讯作者: 沈立松，教授，博士；电子信箱：lisongshen@hotmail.com
杨俊瑶，副研究员，博士；电子信箱：yangjunyao@xinhuamed.com.cn。
作者简介:第一联系人：为共同第一作者（co-first authors）。
基金资助:
国家自然科学基金(81802082);国家自然科学基金(81672363);上海市科技创新行动计划自然科学基金(21ZR1441500);上海交通大学医工交叉项目(YG2025QNB48);上海交通大学医学院附属新华医院院级临床研究创新基金项目(24XHCR04B)

LINC01123 promotes proliferation and glycolysis of gastric cancer via binding to ENO1

ZHANG Shuqiong¹^,²^,³^,⁴, KE Xing¹, ZHAO Xinghe¹, CHEN Xiaocui¹, ZHENG Haodong¹, CHEN Hui¹, SHEN Lisong¹^,²^,³(), YANG Junyao¹^,³^,⁵()

^1.Department of Laboratory Medicine, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China
^2.Faculty of Medical Laboratory Technology, College of Health Science and Technology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China
^3.Institute of Artificial Intelligence Medicine, Shanghai Academy of Experimental Medicine, Shanghai 200092, China
^4.Department of Laboratory Medicine, Shenzhen Second People′s Hospital, Guangdong Province, Shenzhen 518035, China
^5.Clinical Research Unit, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China

Received:2025-05-29 Accepted:2025-06-30 Online:2025-11-28 Published:2025-12-03
Contact: SHEN Lisong, E-mail: lisongshen@hotmail.com
YANG Junyao, E-mail: yangjunyao@xinhuamed.com.cn.
Supported by:
National Natural Science Foundation of China(81802082);Natural Science Foundation of Shanghai Science and Technology Innovation Action Plan(21ZR1441500);Medical Engineering Cross Fund of Shanghai Jiao Tong University(YG2025QNB48);Hospital Funded Clinical Research, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine(24XHCR04B)

摘要/Abstract

摘要：

目的·研究长链非编码RNA LINC01123在胃癌中的表达及其促进肿瘤进展的作用机制，探讨LINC01123成为一种新的胃癌诊断标志物和治疗靶点的可能性。方法·基于癌症基因组图谱（The Cancer Genome Atlas，TCGA）和基因表达综合（Gene Expression Omnibus，GEO）数据库（GSE95667、GSE99416）分析胃癌组织与正常组织中lncRNA的表达差异，使用R语言筛选并确定研究对象LINC01123。利用qRT-PCR验证LINC01123在胃癌细胞系及组织样本中的表达水平。通过基因过表达及敲减，利用CCK-8、克隆形成、划痕实验以及Transwell迁移与侵袭实验体外评估LINC01123对细胞增殖和转移能力的影响；构建裸鼠皮下成瘤模型，观察LINC01123对肿瘤生长的促进作用；检测ATP和乳酸浓度以验证LINC01123对糖酵解的调控能力。进一步通过转录物组测序及基因集富集分析（Gene Set Enrichment Analysis，GSEA）探索其可能参与的分子通路。RNA pull-down联合质谱分析初步筛选LINC01123结合蛋白，结合catRAPID数据库预测并通过蛋白质截断突变体和RNA免疫沉淀（RNA immunoprecipitation，RIP）实验确定关键结合区域；通过功能相互作用实验明确α-烯醇化酶（α-enolase，ENO1）是否介导LINC01123的促肿瘤效应。结果·LINC01123在胃癌组织和细胞中显著高表达，并与患者的不良预后密切相关（P=0.021）。功能实验表明，LINC01123显著促进胃癌细胞如MKN-45细胞的增殖、迁移、侵袭和糖酵解，且在裸鼠体内促进肿瘤生长（均P<0.05）。机制研究显示，LINC01123主要定位于细胞质，并可与ENO1蛋白的第97~237位氨基酸区域直接结合。进一步发现，在LINC01123过表达胃癌细胞中联合敲减ENO1，部分逆转LINC01123介导的胃癌细胞如MKN-45的促增殖和促迁移效应（均P<0.05），提示ENO1增加可增强LINC01123的在胃癌进展中的促进作用。结论·LINC01123在胃癌中呈高表达，并通过与ENO1蛋白结合促进细胞增殖、转移和糖酵解，进而促进肿瘤进展。其有望作为胃癌的新型诊断和预后生物标志物及治疗靶点。

关键词: LINC01123, 胃癌, α-烯醇化酶, 长链非编码RNA, 增殖

Abstract:

Objective ·To investigate the expression and tumor-promoting mechanism of the long non-coding RNA (lncRNA) LINC01123 in gastric cancer and evaluate its potential as a novel diagnostic biomarker and therapeutic target. Methods ·Differential expression analysis of lncRNAs between gastric cancer and normal tissues was performed based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets (GSE95667, GSE99416) by using R software. LINC01123 was identified as the candidate of interest. Its expression was validated in gastric cancer cell lines and clinical tissue samples by using qRT-PCR. The biological effects of LINC01123 on cell proliferation and metastasis were evaluated in vitro through gene overexpression and knockdown by utilizing CCK-8, colony formation, wound healing, and Transwell migration and invasion assays. In vivo, a subcutaneous xenograft tumor model in nude mice was established to assess the effect of LINC01123 on tumor growth. ATP and lactate production were measured to evaluate the role of LINC01123 in glycolysis. Transcriptome sequencing and Gene Set Enrichment Analysis (GSEA) were conducted to explore related pathways. RNA pull-down combined with mass spectrometry was used to identify proteins interacting with LINC01123. The binding region was predicted using the catRAPID database and validated by constructing α-enolase (ENO1) protein truncation mutants and performing RNA immunoprecipitation (RIP) assays. Functional interaction studies were carried out to determine whether ENO1 mediates the oncogenic effect of LINC01123. Results ·LINC01123 was upregulated in gastric cancer tissues and cell lines and was associated with poor patient prognosis (P=0.021). Functional assays demonstrated that LINC01123 promoted proliferation, migration, invasion, and glycolysis of gastric cancer cells such as MKN-45 in vitro, and enhanced tumor growth in vivo (all P<0.05). Mechanistically, LINC01123 was predominantly localized in the cytoplasm and bound to the 97‒237 amino acid region of ENO1 protein. Further studies showed that ENO1 knockdown in LINC01123-overexpressing cells partially reversed the proliferative and migratory effects of LINC01123 (all P<0.05) , indicating that ENO1 upregulation enhances the tumor-promoting function of LINC01123. Conclusion ·LINC01123 is highly expressed in gastric cancer and promotes tumor progression by binding to ENO1 protein and enhancing proliferation, migration, invasion, and glycolysis. LINC01123 holds promise as a novel diagnostic and prognostic biomarker and a potential therapeutic target for gastric cancer.

Key words: LINC01123, gastric cancer, α-enolase, long non-coding RNA, proliferation

中图分类号:

R735.2

张舒琼, 柯星, 赵兴贺, 陈晓翠, 郑浩东, 陈惠, 沈立松, 杨俊瑶. LINC01123通过结合ENO1促进胃癌的增殖和糖酵解[J]. 上海交通大学学报（医学版）, 2025, 45(11): 1443-1457.

ZHANG Shuqiong, KE Xing, ZHAO Xinghe, CHEN Xiaocui, ZHENG Haodong, CHEN Hui, SHEN Lisong, YANG Junyao. LINC01123 promotes proliferation and glycolysis of gastric cancer via binding to ENO1[J]. Journal of Shanghai Jiao Tong University (Medical Science), 2025, 45(11): 1443-1457.

图/表 9

表1 慢病毒载体构建使用的敲减序列

Tab 1 Knockdown sequences for lentiviral vector construction

Gene	Sequence (5′→3′)
si-LINC01123
Sense	TTCTCTTTATTTTTATACAGT
Antisense	ACTGTATAAAAATAAAGAGAA
si-ENO1
Sense	CCCAGUGGUGUCUAUCGAATT
Antisense	UUCGAUAGACACCACUGGGTT
si-NC
Sense	UUCUCCGAACGUGUCACGU
Antisense	ACGUGACACGUUCGGAGAA
sh-LINC01123	CCGGTTCTCTTTATTTTTATACAGTCTCGAGACTGTATAAAAATAAAGAGAATTTTTG
sh-NC	TTCTCCGAACGTGTCACGT

表2 qRT-PCR引物序列

Tab 2 Primers sequences for qRT-PCR

Gene	Sequence (5′→3′)
LINC01123
Forward	ACAGTGGCCGCACGCATAGCTG
Reverse	CTGACGACCGAGGTGACAACGATGA
ENO1
Forward	GCCTCCTGCTCAAAGTCAAC
Reverse	AACGATGAGACACCATGACG
GAPDH
Forward	TTGGTATCGTGGAAGGACTCA
Reverse	TGTCATCATATTTGGCAGGTTT
U6
Forward	CGCTTCGGCAGCACATATAC
Reverse	TTCACGAATTTGCGTGTCATC

图1 LINC01123在胃癌中的高表达及不良预后关联Note： A/B. Venn diagrams illustrating the overlap of upregulated (A) and downregulated (B) long non-coding RNAs (lncRNAs) identified in the TCGA-STAD, GSE95667, and GSE99416 datasets. C. Volcano plot depicting differentially expressed lncRNAs in the TCGA-STAD dataset. D. LINC01123 expression was significantly upregulated in gastric cancer cell lines. E. LINC01123 expression was significantly upregulated in gastric cancer tissues compared to adjacent normal tissues. F. Expression of LINC01123 across different cancer types in TCGA. G. UALCAN analysis showing that LINC01123 was upregulated in STAD tissues. H. LINC01123 expression in different TNM stages of gastric cancer. I. LINC01123 expression profile based on tumor histology. J. Kaplan-Meier analysis showing that high LINC01123 expression was associated with poor overall survival in TCGA-STAD patients. K. Gene set enrichment analysis (GSEA) comparing high and low LINC01123 expression groups. ①P=0.011, ②P=0.002, ③P=0.007, compared with GES-1; ④P<0.001, ⑤P=0.004, compared with Normal.

Fig 1 Overexpression of LINC01123 in gastric cancer and its association with poor prognosis

图2 LINC01123敲低对胃癌细胞体外增殖、迁移和侵袭的抑制作用Note： A. qRT-PCR assay demonstrated that sh-LINC01123 lentivirus effectively altered LINC01123 expression. B/C. CCK-8 assay (B) and colony-formation assay (C) showed the effects of knockdown of LINC01123 on cell proliferation. D/E. Wound healing assay (D) and Transwell migration assay (E) were performed to detect the migration ability of MKN-45 and AGS cells after knockdown of LINC01123. F. Transwell invasion assay was conducted to assess the effects of LINC01123 knockdown on cell invasion. ①P=0.030, ②P=0.011, ③P<0.001, ④P=0.010, ⑤P=0.020, ⑥P=0.009, ⑦P=0.005, ⑧P=0.007, compared with sh-NC.

Fig 2 Inhibitory effects of LINC01123 knockdown on gastric cancer cell proliferation, migration, and invasion in vitro

图3 LINC01123过表达对胃癌细胞体外增殖、迁移和侵袭的促进作用Note： A. qRT-PCR assay demonstrated that LINC01123 overexpression lentivirus effectively altered LINC01123 expression. B/C. CCK-8 assay (B) and colony-formation assay (C) showed the effects of overexpression of LINC01123 on cell proliferation. D. Wound healing assay was performed to detect the migration ability of MKN-45 and HGC-27 cells after the overexpression of LINC01123. E. Transwell migration assay was performed to detect the migration ability of MKN-45 and HGC-27 cells after the overexpression of LINC01123. F. Transwell invasion assay was conducted to assess the effects of knockdown or overexpression of LINC01123 on cell invasion. ①P<0.001, ②P=0.006, ③P=0.007, ④P=0.010, ⑤P=0.020, ⑥P=0.009, ⑦P=0.030, ⑧P=0.002, ⑨P=0.005, compared with Vector.

Fig 3 Promotive effects of LINC01123 overexpression on gastric cancer cell proliferation, migration, and invasion in vitro

图4 LINC01123对EMT及PI3K/AKT信号通路的调控作用Note：A. Volcano plot of differentially expressed lncRNAs. B. KEGG enrichment results of differentially expressed genes in MKN-45 cells transfected with si-NC and si-LINC01123. C. GO enrichment results of differentially expressed genes in MKN-45 cells transfected with si-NC and si-LINC01123. D. Heatmap of genes defining epithelial-mesenchymal transition (EMT). E. Heatmap of genes up-regulated by activation of the PI3K/AKT/mTOR pathway.

Fig 4 Regulatory role of LINC01123 in EMT and PI3K/AKT pathway

图5 LINC01123在体内促进胃癌MKN-45细胞的成瘤能力Note： A. Representative images of nude mice subcutaneously injected with MKN-45 cells stably expressing sh-NC or sh-LINC01123 lentivirus (n=5 per group). B. Excised tumors from nude mice in sh-NC and sh-LINC01123 groups. C. Tumor volumes of two groups were assessed for 26 d. D. Tumor weight of two groups. ①P<0.001, ②P=0.002, compared with sh-NC.

Fig 5 Promotion of tumorigenesis of gastric cancer MKN-45 cells by LINC01123 in vivo

图6 LINC01123与ENO1蛋白的结合及对胃癌细胞糖酵解的调节作用Note： A. Expression of LINC01123 in the cytoplasm and nucleus of gastric cancer cells. B. Fluorescence in situ hybridization (FISH) assay showing the localization of LINC01123 in MKN-45 cells. C. Silver-stained SDS-PAGE of proteins from RNA pull-down assay of MKN-45 cell extracts. The red arrow indicates the band used for mass spectrometry analysis. D. ENO1 pulled down by LINC01123 and negative control RNA was analyzed by Western blotting. Input represents the total protein used for RNA pull-down. E. PCR analysis of LINC01123 expression from RNA immunoprecipitation (RIP) assays. F. Co-staining of LINC01123 (green) and ENO1 (red) in MKN-45 cells by in FISH. G. Schematic map of the potential binding site of LINC01123 in ENO1 by catRAPID analysis. H. The interaction matrix between LINC01123 and ENO1 by catRAPID fragments analysis. I. Graphic display of ENO1 and its truncations. J. Flag-tagged ENO1 and its truncations were verified by Western blotting. K. Quantitative PCR of LINC01123 from purified RNAs of RIP experiments performed with 293T cell extracts transfected with Flag-tagged ENO1 or its truncations. L. Reduced lactate production in MKN-45 and AGS cells after LINC01123 knockdown. M. Reduced ATP production in MKN-45 and AGS cells after LINC01123 knockdown. ①P=0.002, ②P<0.001, compared with IgG; ③P<0.001, ④P=0.009, ⑤P=0.001, compared with sh-NC.

Fig 6 Binding of LINC01123 to ENO1 protein and regulation of glycolysis in gastric cancer cells by LINC01123

图7 LINC01123通过ENO1发挥的促增殖、迁移、侵袭和糖酵解功能Note： A. ENO1 expression after transfection of ENO1 siRNA in LINC01123-overexpressing gastric cancer MKN-45 and HGC-27 cell lines. B. CCK-8 assay showing that the proliferation of MKN-45 and HGC-27 cells overexpressing LINC01123 decreased after ENO1 knockdown. C. Wound healing assay showing that the migration of MKN-45 and HGC-27 cells overexpressing LINC01123 decreased after ENO1 knockdown. D. Transwell migration assay showing that the migration of MKN-45 cells overexpressing LINC01123 decreased after interference with ENO1 expression. E. Transwell invasion assay showing that the invasion of MKN-45 cells overexpressing LINC01123 decreased after ENO1 knockdown. F/G. ENO1 knockdown reduces LINC01123-induced lactate production (F) and ATP production (G) in MKN-45 and HGC-27 cells overexpressing LINC01123. ①P<0.001, ②P=0.008, ③P=0.006, ④P=0.001, ⑤P=0.007, ⑥P=0.002, ⑦P=0.012, ⑧P=0.020, ⑨P=0.011, ⑩P=0.004.

Fig 7 Promotion of proliferation, migration, invasion, and glycolysis by LINC01123 via ENO1

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LINC01123通过结合ENO1促进胃癌的增殖和糖酵解

LINC01123 promotes proliferation and glycolysis of gastric cancer via binding to ENO1

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