安五脂素通过拮抗JAK1/STAT3通路的激活抑制胃癌细胞恶性生物学行为

doi:10.12122/j.issn.1673-4254.2026.09.22

南方医科大学学报 ›› 2026, Vol. 46 ›› Issue (9): 2242-2257.doi: 10.12122/j.issn.1673-4254.2026.09.22

• • 上一篇

安五脂素通过拮抗JAK1/STAT3通路的激活抑制胃癌细胞恶性生物学行为

刘馨悦¹^,⁴(), 张可妮², 乔通³, 尹林², 张龙涛³, 程歆柯¹^,⁴, 王奔¹^,⁴, 曹锦麟¹^,⁴, 耿志军¹^,⁴, 赵皓¹()

^1.蚌埠医科大学第一附属医院，中心实验室，安徽蚌埠 233004
^2.蚌埠医科大学第一附属医院，检验科，安徽蚌埠 233000；蚌埠医科大学，安徽蚌埠 233004
^3.蚌埠医科大学第一附属医院，检验医学院免疫学教研室，安徽蚌埠 233004
^4.蚌埠医科大学第一附属医院，炎症相关性疾病基础与转化研究安徽省重点实验室，安徽蚌埠 233004

收稿日期:2025-12-20 出版日期:2026-09-20 发布日期:2026-09-30
通讯作者: 赵皓 E-mail:lxy13865038871@163.com;13955221252@163.com
作者简介:刘馨悦，在读本科生，E-mail: lxy13865038871@163.com
基金资助:
安徽省高校优秀青年基金项目(2022AH030138);安徽省高等学校自然科研究项目(KJ2020A0563)

Anwulignan inhibits malignant phenotypes of gastric cancer cells by antagonizing activation of the JAK1/STAT3 signaling pathway

Xinyue LIU¹^,⁴(), Keni ZHANG², Tong QIAO³, Lin YIN², Longtao ZHANG³, Xinke CHENG¹^,⁴, Ben WANG¹^,⁴, Jinlin CAO¹^,⁴, Zhijun GENG¹^,⁴, Hao ZHAO¹()

^1.Central Laboratory, First Affiliated Hospital of Bengbu Medical University, Bengbu 233003, China
^2.Clinical Laboratory, First Affiliated Hospital of Bengbu Medical University, Bengbu 233003, China
^3.Department of Immunology, School of Laboratory Medicine, Bengbu Medical University, Bengbu 233000, China
^4.Anhui Provincial Key Laboratory of Basic and Translational Research of Inflammation-related Diseases, Bengbu 233003, China

Received:2025-12-20 Online:2026-09-20 Published:2026-09-30
Contact: Hao ZHAO E-mail:lxy13865038871@163.com;13955221252@163.com

摘要/Abstract

摘要：

目的明确安五脂素（ANW）对胃癌细胞恶性生物学行为的调控作用，并探讨其潜在分子机制。方法采用CCK-8法、EdU染色及克隆形成实验评估ANW对人胃癌细胞系HGC-27和SGC-7901活力与增殖能力的影响；构建裸鼠移植瘤模型，结合Ki-67免疫组化染色验证ANW对胃癌细胞体内增殖的作用。通过流式细胞术检测细胞周期分布，Western blotting检测周期相关蛋白（Cyclin D1、CDK2、P53）表达；采用Annexin V-FITC/PI双染流式细胞术检测细胞凋亡率，TUNEL法标记凋亡细胞，Western blotting检测凋亡相关蛋白（Cleaved Caspase-3、Bcl-2、Bax）表达。利用Transwell检测细胞迁移与侵袭能力，Western blotting检测基质金属蛋白酶（MMP-2、MMP-9）表达。通过qPCR和Western blotting检测上皮-间质转化（EMT）标志分子（Vimentin、E-cadherin、Snail、Slug）的mRNA及蛋白表达水平；Western blotting分析JAK1/STAT3信号通路关键蛋白（p-JAK1、JAK1、p-STAT3、STAT3）的磷酸化水平，联合RO8191通路激活及JAK1 siRNA敲低实验，验证JAK1/STAT3通路是ANW抗肿瘤作用的关键介导通路。结果 ANW以浓度依赖方式显著抑制HGC-27和SGC-7901增殖及克隆形成能力（P<0.05），并诱导细胞周期阻滞于G1期，伴随Cyclin D1、CDK2蛋白表达下调及P53蛋白表达降低（P<0.05）。体内实验进一步证实，ANW可抑制裸鼠移植瘤生长，降低瘤体组织中Ki-67阳性表达率（P<0.05）。ANW可显著促进胃癌细胞凋亡，表现为凋亡率升高，抗凋亡蛋白Bcl-2表达下调，促凋亡蛋白Cleaved Caspase-3及Bax表达上调（P<0.05）。此外，ANW能显著抑制胃癌细胞迁移与侵袭能力，同时下调MMP-2、MMP-9蛋白表达（P<0.05）；并可抑制EMT进程，具体表现为间质标志物Vimentin及转录因子Snail、Slug表达降低，上皮标志物E-cadherin表达升高（P<0.05）。分子机制层面，ANW可显著抑制JAK1及STAT3的磷酸化水平（P<0.05）；JAK1/STAT激活剂RO8191可逆转ANW对胃癌细胞恶性行为的抑制作用，siRNA沉默JAK1既可模拟ANW的抗肿瘤效应，又能与之协同；ANW在裸鼠移植瘤中抑制EMT，而RO8191则削弱其体内抑瘤作用。结论安五脂素可通过抑制JAK1/STAT3信号通路的活化，进而阻滞细胞周期进程、促进细胞凋亡、抑制EMT及MMPs介导的侵袭迁移能力，最终发挥抗胃癌作用。本研究为ANW作为胃癌潜在治疗药物的开发提供了实验依据。

关键词: 胃癌, 安五脂素, 恶性行为, 上皮间质转化, JAK1/STAT3通路

Abstract:

Methods To evaluate the inhibitory effect of anwulignan (ANW) on malignant biological behaviors of gastric cancer cells and explore its underlying molecular mechanism. Methods The inhibitory effect of ANW on viability and proliferation of gastric cancer HGC-27 and SGC-7901 cells were evaluated using CCK-8 assay, EdU staining and colony formation assay. In a nude mouse model bearing gastric cancer xenografts, the effect of ANW on tumor cell proliferation was examined using immunohistochemistry for Ki-67. The changes in cell cycle, apoptosis, migration, invasion, and expressions of MMPs and epithelial-mesenchymal transition (EMT) markers following ANW treatment were detected using flow cytometry, TUNEL staining, Western blotting, Transwell assay, and qPCR. The role of the JAK1/STAT3 signaling pathway in mediating the anti-tumor activity of ANW was validated by detecting JAK1/STAT3 phosphorylation, pathway activation and siRNA-mediated JAK1 knockdown experiments. Results In HGC-27 and SGC-7901 cells, ANW dose-dependently suppressed cell proliferation and colony formation, induced G1 cell cycle arrest, and downregulated the expressions of cyclin D1/CDK2 and P53. ANW treatment significantly inhibited tumor growth and decreased Ki-67 positivity in the mouse xenografts. ANW effectively promoted cell apoptosis, suppressed Bcl-2 expression, upregulated cleaved caspase-3 and Bax expressions, inhibited migration and invasion, lowered MMP-2/MMP-9 expressions, and blocked EMT progression in gastric cancer cells. Mechanistically, ANW significantly inhibited JAK1/STAT3 phosphorylation, while the JAK1/STAT3 activator RO8191 reversed the anti-tumor effect of ANW; JAK1 knockdown mimicked and enhanced the inhibitory effect of ANW on gastric cancer cells. ANW significantly inhibited EMT in the mouse xenografts, and this effect was attenuated by RO8191 treatment. Conclusion ANW inhibits malignant phenotype of gastric cancer cells by inhibiting the activation of the JAK1/STAT3 signaling pathway, thereby inducing cell cycle arrest, promoting apoptosis, and suppressing EMT and MMP-mediated invasion and migration, suggesting the potential of ANW as a therapeutic agent for gastric cancer.

Key words: gastric cancer, anwuligan, malignant behavior, epithelial-mesenchymal transition, JAK1/STAT3 signaling pathway

刘馨悦, 张可妮, 乔通, 尹林, 张龙涛, 程歆柯, 王奔, 曹锦麟, 耿志军, 赵皓. 安五脂素通过拮抗JAK1/STAT3通路的激活抑制胃癌细胞恶性生物学行为[J]. 南方医科大学学报, 2026, 46(9): 2242-2257.

Xinyue LIU, Keni ZHANG, Tong QIAO, Lin YIN, Longtao ZHANG, Xinke CHENG, Ben WANG, Jinlin CAO, Zhijun GENG, Hao ZHAO. Anwulignan inhibits malignant phenotypes of gastric cancer cells by antagonizing activation of the JAK1/STAT3 signaling pathway[J]. Journal of Southern Medical University, 2026, 46(9): 2242-2257.

图/表 15

表1 RT-qPCR的引物序列

Tab.1 Primer sequences for RT-qPCR

Gene	Forward (5'-3')	Reverse (5'-3')
Vimentin	TCTATACCACTTCACAAGTCGGA	GAATTGCCATTGCACAACTCTTT
CDH1	GATAGAGAACGCATTGCCACATA	ACCTTCCATGACAGACCCCTTAA
GAPDH	TGAAGGTCGGAGTCAACGGAT	CTGGAAGATGGTGATGGGATT

图1 ANW对胃癌细胞增殖的影响

Fig.1 Effect of ANW on proliferation of gastric cancer cells in vitro. A, B: Cell viability detected by CCK-8 assay. C-E, H: Colony formation assay. F, G, I, J: EdU assay for evaluating cell proliferation. *P<0.05 vs Control (0 μmol/L). ANW: Anwulignan; Con: Control; EdU: 5-ethynyl-2'-deoxyuridine.

图2 ANW对裸鼠移植瘤生长的抑制作用

Fig.2 Inhibitory effect of ANW on xenograft tumor growth in nude mice. A-C: Tumor volume and weight. D: Representative images and quantitative analysis of Ki-67 staining. *P<0.05 vs Control (0 μmol/L).

图3 ANW对胃癌细胞周期的影响

Fig.3 Effect of ANW on cell cycle in gastric cancer cells'. A-D: Flow cytometric analysis of cell cycle distribution. E-H: Western blotting analysis of cyclin D1, CDK2, and P53 protein expression in gastric cancer cell lines HGC 27 and SGC 7901. I, J: Western blotting analysis of cyclin D1, CDK2, and P53 protein expression in mouse xenografts. *P<0.05 vs Control (0 μmol/L). Cyclin-D1: G1/S-specific cyclin-D1; CDK2: Cyclin-dependent kinase 2; P53: Tumor protein p53; β-actin: Beta actin.

图4 流式细胞术分析ANW对胃癌细胞凋亡的影响

Fig.4 Flow cytometric analysis of the effects of ANW on apoptosis in gastric cancer cells. A-D: Cell aspoptosis rates detected by flow cytometry. *P<0.05 vs Control (0 μmol/L).

图5 Western blotting和Tunel分析ANW对胃癌细胞凋亡的影响

Fig.5 Western blotting and TUNEL analysis of the effects of ANW on apoptosis in gastric cancer cells. A-D: Western blotting analysis of apoptosis-related proteins gastric cancer cells in vitro. E, F: Western blotting analysis of apoptosis-related proteins in mouse xenografts. G, H: TUNEL staining of xenograft tissues. *P<0.05 vs Control (0 μmol/L).

图6 Transwell和划痕实验分析ANW对胃癌细胞迁移和侵袭的影响

Fig.6 Transwell and wound healing assays of migration and invasion in ANW-treated gastric cancer cells. A-C, E: Transwell migration and invasion assay. D, F, G, H: Wound healing assay. *P<0.05 vs Control (0 μmol/L).

图7 Western blotting分析ANW对胃癌细胞迁移和侵袭的影响

Fig.7 Western blotting for evaluating the effects of ANW on migration and invasion in gastric cancer cells. A, B: Western blotting and quantification of MMP2 and MMP9 expressions in gastric cancer cells in vitro. C: Western blotting and quantification of MMP2 and MMP9 expressions in mouse xenografts. *P<0.05 vs Control (0 μmol/L). MMP2: Matrix Metalloproteinase 2; MMP9: Matrix Metalloproteinase 9.

图8 Transwell分析RO8191对ANW抑制胃癌细胞恶性表型及EMT的影响

Fig.8 Transwell analysis of the effects of RO8191 on the inhibitory action of ANW on malignant phenotype and EMT in gastric cancer cells. A-C: Transwell migration and invasion assay. *P<0.05 vs Control; #P<0.05 vs ANW.

图9 Western blotting分析RO8191对ANW抑制胃癌细胞恶性表型及EMT的影响

Fig.9 Western blotting analysis of the effects of RO8191 on the inhibitory action of ANW on malignant phenotype and EMT in gastric cancer cells. A-H: The expression of proteins related to migration, invasion, apoptosis, and EMT. *P<0.05 vs Control; #P<0.05 vs ANW.

图10 ANW对胃癌细胞上皮间质转化的影响

Fig.10 Effect of ANW on epithelial-mesenchymal transition in gastric cancer cells. A-C: Western blotting of EMT-related proteins in vitro and in vivo. D: RT-qPCR analysis of EMT-related gene expression. *P<0.05 vs Control (0 μmol/L). Snail+slug: Snail family zinc finger transcription factors; E-cad: Epithelial cadherin; VIM: Vimentin; CDH1: Cadherin 1.

图11 ANW对JAK1/STAT3信号通路的影响

Fig.11 Effect of ANW on the JAK1/STAT3 signaling pathway. A, B: Western blotting of p-JAK1, JAK1, p-STAT3, and STAT3 in vitro. C: Western blotting analysis of pathway proteins in vivo. *P<0.05vs Control (0 μmol/L). p-STAT3: Phosphorylated signal transducer and activator of transcription 3; STAT3: Signal transducer and activator of transcription 3; p-JAK1: Phosphorylated Janus kinase 1; JAK1: Janus kinase 1.

图12 Transwell分析沉默JAK1/STAT3通路对ANW抑制胃癌细胞恶性表型及EMT的影响

Fig.12 Transwell analysis of the effects of JAK1/STAT3 pathway silencing on the inhibitory action of ANW on malignant phenotype and EMT in gastric cancer cells. A-C: Transwell migration and invasion assay. *P<0.05 vs Control; #P<0.05 vs ANW.

图13 WB分析沉默JAK1/STAT3通路对ANW抑制胃癌细胞恶性表型及EMT的影响

Fig.13 Western blotting of the effects of JAK1/STAT3 pathway silencing on the inhibitory action of ANW on malignant phenotype and EMT in gastric cancer cells. A-H: Expression of proteins related to migration, invasion, apoptosis, and EMT. *P<0.05 vs Control; #P<0.05 vs ANW.

图14 裸鼠体内通路机制验证

Fig.14 Validation of pathway mechanism in nude mice. A-C: Tumor volume and weight. D: Expression of proteins related to EMT. *P<0.05 vs Control; #P<0.05 vs ANW.

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安五脂素通过拮抗JAK1/STAT3通路的激活抑制胃癌细胞恶性生物学行为

Anwulignan inhibits malignant phenotypes of gastric cancer cells by antagonizing activation of the JAK1/STAT3 signaling pathway

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