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BAP31 通过激活 PI3K/AKT 通路促进肝癌细胞的增殖、侵袭和转移。

BAP31 Promotes Proliferation, Invasion, and Metastasis of Liver Cancer Cells via Activating PI3K/AKT Pathway.

机构信息

Department of Hepatic Surgery I, The Third Affiliated Hospital of Naval Military Medical University, Shanghai 200438, China.

Department of Radioactive Intervention, The Third Affiliated Hospital of Naval Military Medical University, Shanghai 200438, China.

出版信息

J Healthc Eng. 2022 Apr 11;2022:7686728. doi: 10.1155/2022/7686728. eCollection 2022.

Abstract

BACKGROUND

Many breakthroughs have been made in the clinical treatment of liver cancer, but there are still many liver cancer patients with limited treatment methods. Therefore, it is very important to find targets for early diagnosis and specific treatment of liver cancer.

METHODS

During the operation, 32 pairs of tumor tissues and corresponding normal liver tissues were acquired from patients. The mRNA expression was measured by qPCR. The protein expression was evaluated via Western blot. Flow cytometry assay was performed to measure the cells apoptosis. CCK-8 assay was performed to detect cell proliferation. Transwell chamber assay was applied to detect migration and invasion of SNU-449 cells.

RESULTS

BAP31 was upregulated in liver cancer tissues and cells. Knockdown of BAP31 repressed cell proliferation and enhanced cell apoptosis of liver cancer. Knockdown of BAP31 apparently upregulated apoptosis-related proteins (Bax and Caspase-3), while it downregulated antiapoptotic proteins (Bcl-2). Knockdown of BAP31 repressed migration and invasion of SNU-449 cells. In contrast with the control and si-NC group, protein expression of MMP-2 and MMP-9 was obviously lower after si-BAP31 transfection of cells. Knockdown of BAP31 repressed PI3K/AKT signaling pathways in liver cancer cells.

CONCLUSION

Knockdown of BAP31 repressed cell proliferation, migration, and invasion in liver cancer by suppressing PI3K/AKT/mTOR signaling pathways.

摘要

背景

肝癌的临床治疗已经取得了许多突破,但仍有许多肝癌患者治疗方法有限。因此,寻找肝癌早期诊断和特异性治疗的靶点非常重要。

方法

在手术过程中,从患者中获得 32 对肿瘤组织和相应的正常肝组织。通过 qPCR 测量 mRNA 表达。通过 Western blot 评估蛋白质表达。通过流式细胞术测定细胞凋亡。通过 CCK-8 测定检测细胞增殖。通过 Transwell 室测定检测 SNU-449 细胞的迁移和侵袭。

结果

BAP31 在肝癌组织和细胞中上调。BAP31 的敲低抑制肝癌细胞的增殖并增强细胞凋亡。BAP31 的敲低明显上调凋亡相关蛋白(Bax 和 Caspase-3),同时下调抗凋亡蛋白(Bcl-2)。BAP31 的敲低抑制 SNU-449 细胞的迁移和侵袭。与对照组和 si-NC 组相比,si-BAP31 转染细胞后 MMP-2 和 MMP-9 的蛋白表达明显降低。BAP31 的敲低抑制肝癌细胞中的 PI3K/AKT 信号通路。

结论

BAP31 的敲低通过抑制 PI3K/AKT/mTOR 信号通路抑制肝癌细胞的增殖、迁移和侵袭。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc64/9017443/c70f291fa08f/JHE2022-7686728.001.jpg

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