异隐托平通过m6A介导的Hedgehog信号通路对口腔鳞状细胞癌增殖和上皮-间质转化的影响

Junxia Gong, Chunlin Wang, Fang Zhang, Weidong Lan
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引用次数: 1

摘要

背景:异隐碱是一种从麦草属植物中提取的异喹啉类生物碱。本研究旨在探讨异隐托平对口腔鳞癌(OSCC)细胞生长和转移的影响。方法选择人OSCC细胞系HSC-3和SAS。MTT法测定细胞活力。Western blot检测蛋白表达。Transwell法检测细胞迁移和浸润情况。甲基化RNA免疫沉淀法证实M6A修饰。结果与NC组比较,异隐托平对OSCC细胞活力、迁移和侵袭能力均有一定的抑制作用,且呈剂量依赖性。异隐topine上调OSCC细胞中E-cadherin的表达,下调N-cadherin和Vimentin的表达。此外,异隐碱处理后,斑块受体1 (PTCH1)、平滑共受体(SMO)和Gli家族(GLI1)蛋白表达下调。此外,异隐碱处理降低了甲基转移酶如3 (METTL3)的表达,抑制了PTCH1的n6 -甲基腺苷(m6A)修饰。此外,PTCH1的过表达逆转了异隐托平的作用,并诱导了OSCC细胞的侵袭性。结论异隐topine通过m6A介导的Hedgehog信号通路抑制OSCC细胞的增殖和上皮间质转化(epithelial-mesenchymal transition, EMT),减轻OSCC的致癌行为。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of Allocryptopine on the Proliferation and Epithelial-Mesenchymal Transition of Oral Squamous Cell Carcinoma through m6A Mediated Hedgehog Signaling Pathway.
BACKGROUND Allocryptopine is an isoquinoline alkaloid extracted from Macleaya cordata. This study aimed to explore the effects of allocryptopine on the growth and metastasis of oral squamous cell carcinoma (OSCC) cells. METHODS The human OSCC cell line HSC-3 and SAS were selected in this study. MTT assay was performed to measure cell viability. Western blot was used to detect protein expressions. transwell assay was conducted to determine the migrated and invaded cells. M6A modification was confirmed by methylated RNA immunoprecipitation assay. RESULTS Compared with the NC group, the cell viability, migration and invasion ability of OSCC cells were suppressed after allocryptopine treatment in a dose dependent manner. Allocryptopine upregulated the E-cadherin expression and downregulated N-cadherin and Vimentin expressions in the OSCC cells. In addition, the protein expressions of patched receptor 1 (PTCH1), smoothened co-receptor (SMO) and Gli family (GLI1) were downregulated after allocryptopine treatment. Furthermore, allocryptopine treatment decreased the expression of Methyltransferase like 3 (METTL3) and inhibited N6-methyladenosine (m6A) modification of PTCH1. Moreover, overexpression of PTCH1 reversed the effects of allocryptopine and induced the aggressiveness of OSCC cells. CONCLUSION Allocryptopine suppressed the proliferation and epithelial-mesenchymal transition (EMT) of OSCC cells via m6A mediated Hedgehog signaling pathway, relieving the carcinogenic behaviors of OSCC.
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