Radioactive ¹²⁵I Seed Inhibits Cell Migration and Invasion and Promotes Apoptosis by Inactivating the VEGFR2 Signaling Pathway in Cholangiocarcinoma.

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS ACS Applied Bio Materials Pub Date : 2023-07-01 DOI:10.1177/15593258231187348

Jun Luo, Jiaping Zheng, Hongxiang Yao, Binbing Wang, Zhewei Zhang, Guoliang Shao

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Abstract

Objectives: To investigate the potential mechanisms of ¹²⁵I seed implantation therapeutic treatment on inactivating the VEGFR2/PI3K/AKT pathway in cholangiocarcinoma.

Methods: The human cholangiocarcinoma cell lines HCCC-9810 and HuCCT1 were purchased for in vitro studies. The BALB/c nude mice were obtained for in vivo studies. The proliferation of cells was detected by CCK-8, colony formation, and BrdU staining. The migration and invasion of cells were determined by wound healing assay and Transwell assay, respectively. Hematoxylin and eosin staining was utilized for histological evaluation. Protein expression was determined by western blotting and immunohistochemistry.

Results: Compared with the control group, .6 mCi group and .8 mCi group inhibited cholangiocarcinoma cells proliferation, invasion, migration, and promoted apoptosis, the protein expression of p-VEGFR2, VEGFR2, PI3K, p-AKT/AKT, cyclin B1, cyclin A, CDK1, and Bcl-2 was decreased. Similar results were obtained from in vitro experiments. However, when VEGF is overexpressed, the inhibitory effect of .8 mCi was partially significantly reversed on cholangiocarcinoma cells. The in vivo studies further confirmed the inhibitory effects of .6 mCi group and .8 mCi group on cholangiocarcinoma.

Conclusion: ¹²⁵I seed irradiation could inhibit cholangiocarcinoma cells proliferation, migration, and invasion and promote apoptosis through inactivation of the VEGFR2/PI3K/AKT signaling pathway.

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放射性125I种子通过失活VEGFR2信号通路抑制胆管癌细胞迁移和侵袭并促进细胞凋亡

目的:探讨125I粒子植入治疗对胆管癌中VEGFR2/PI3K/AKT通路失活的潜在机制。方法:购买人胆管癌细胞株HCCC-9810和HuCCT1进行体外研究。获得BALB/c裸鼠进行体内研究。CCK-8、菌落形成、BrdU染色检测细胞增殖情况。采用创面愈合法和Transwell法测定细胞的迁移和侵袭。采用苏木精和伊红染色进行组织学评价。western blotting和免疫组织化学检测蛋白表达。结果:与对照组相比，.6 mCi组和.8 mCi组抑制了胆管癌细胞的增殖、侵袭、迁移，促进了细胞凋亡，p-VEGFR2、VEGFR2、PI3K、p-AKT/AKT、cyclin B1、cyclin A、CDK1、Bcl-2蛋白表达降低。体外实验也得到了类似的结果。然而，当VEGF过表达时，0.8 mCi对胆管癌细胞的抑制作用被部分显著逆转。体内研究进一步证实了0.6 mCi组和0.8 mCi组对胆管癌的抑制作用。结论:125I种子辐照可通过使VEGFR2/PI3K/AKT信号通路失活，抑制胆管癌细胞的增殖、迁移、侵袭，促进细胞凋亡。

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