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野黄芩苷通过 Wnt/β-连环蛋白信号通路抑制胃癌细胞增殖并诱导其凋亡。

Scutellarin Suppressed Proliferation and Induced Apoptosis in Gastric Cancer via Wnt/β-catenin Signaling Pathway.

机构信息

Department of Endoscopy Center, Nanjing Hospital of Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Nanjing, Jiangsu Province, 210004, China.

Department of Gastroenterology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, 210004, China.

出版信息

Curr Pharm Des. 2023;29(5):368-378. doi: 10.2174/1381612829666230130141931.

DOI:10.2174/1381612829666230130141931
PMID:36717995
Abstract

BACKGROUND

Scutellarin exerts anticancer effects on diverse malignancies. However, its function in gastric cancer has not been explored.

OBJECTIVE

This study aimed to examine the anticancer effect and molecular mechanism of scutellarin in gastric cancer.

MATERIALS AND METHODS

Gastric cancer cells were treated with scutellarin and transfected with the Wnt1 overexpression plasmid. Cell viability, proliferation, toxicity, and apoptosis were determined by cell counting kit-8 (CCK-8), colony formation, lactate dehydrogenase (LDH) activity, TdT-mediated dUTP Nick-End Labeling (TUNEL), and flow cytometry assays. Expressions of apoptosis-related and Wnt/β-catenin signaling pathway- related proteins were examined by western blot and quantitative reverse transcription polymerase chain reaction (qRT-PCR).

RESULTS

Scutellarin concentration dependently restrained cell viability. Scutellarin (20 and 80 μmol/L) suppressed proliferation and promoted LDH release and apoptosis. Moreover, scutellarin elevated Bax and Cytochrome C levels but diminished the levels of Bcl-2, Wnt1, cytoplasmic β-catenin, and basal cytoplasmic β- catenin. However, the above-mentioned regulatory effects of scutellarin were all reversed by Wnt1 overexpression.

CONCLUSION

Scutellarin suppressed gastric cancer cell proliferation and promoted apoptosis by inhibition of the Wnt/β-catenin pathway.

摘要

背景

野黄芩苷对多种恶性肿瘤具有抗癌作用。然而,其在胃癌中的作用尚未得到探索。

目的

本研究旨在研究野黄芩苷在胃癌中的抗癌作用和分子机制。

材料和方法

用野黄芩苷处理胃癌细胞,并转染 Wnt1 过表达质粒。通过细胞计数试剂盒-8(CCK-8)、集落形成、乳酸脱氢酶(LDH)活性、末端转移酶介导的 dUTP 缺口末端标记(TUNEL)和流式细胞术检测细胞活力、增殖、毒性和细胞凋亡。通过 Western blot 和定量逆转录聚合酶链反应(qRT-PCR)检测凋亡相关和 Wnt/β-catenin 信号通路相关蛋白的表达。

结果

野黄芩苷浓度依赖性地抑制细胞活力。野黄芩苷(20 和 80 μmol/L)抑制增殖并促进 LDH 释放和细胞凋亡。此外,野黄芩苷增加 Bax 和细胞色素 C 的水平,但降低 Bcl-2、Wnt1、细胞质 β- catenin 和基础细胞质 β- catenin 的水平。然而,Wnt1 的过表达逆转了野黄芩苷的上述调节作用。

结论

野黄芩苷通过抑制 Wnt/β-catenin 通路抑制胃癌细胞增殖并促进细胞凋亡。

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