Knockdown of AMIGO2 suppresses proliferation and migration through regulating PPAR-γ in bladder cancer.

IF 2.7 3区生物学

Hereditas Pub Date : 2024-07-08 DOI:10.1186/s41065-024-00325-z

Dali Han, Bin Xiong, Xiangxiang Zhang, Chaohu Chen, Zhiqiang Yao, Hao Wu, Jinlong Cao, Jianpeng Li, Pan Li, Zhiping Wang, Junqiang Tian

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引用次数: 0

Abstract

Purpose: This study aims to reveal the relationship between AMIGO2 and proliferation, migration and tumorigenicity of bladder cancer, and explore the potential molecular mechanisms.

Methods: The expression level of AMIGO2 is measured by qRT-PCR and immunohistochemistry (IHC). Stable AMIGO2 knockdown cell lines T24 and 5637 were established by lentivirus transfection. Cell Counting Kit (CCK-8 assay) was produced to determine cell proliferation, flow cytometry analysis was utilized to detect cell cycle, and wound healing assay was proceeded to test migration ability of bladder cancer cells. Xenograft mouse model was established for investigating the effect of AMIGO2 on tumor formation in vivo. The RNA Sequencing technology was applied to explore the underlying mechanisms. The expression level of PPAR-γ was measured by Western Blot.

Results: AMIGO2 was upregulated in bladder cancer cells and tissues. Inhibited expression of AMIGO2 suppresses cell proliferation and migration. Low AMIGO2 expression inhibited tumorigenicity of 5637 in nude mice. According to RNA-Seq and bioinformatics analysis, 917 DEGs were identified. The DEGs were mainly enriched in cell-cell adhesion, peroxisome proliferators-activated receptors (PPARs) signaling pathway and some other pathways. PPAR-γ is highly expressed in bladder cancer cell lines T24 and 5637, but when AMIGO2 is knocked down in T24 and 5637, the expression level of PPAR-γ is also decreased, and overexpression of PPAR-γ could reverse the suppression effect of cell proliferation and migration caused by the inhibition of AMIGO2.

Conclusion: AMIGO2 is overexpressed in bladder cancer cells and tissues. Knockdown of AMIGO2 suppresses bladder cancer cell proliferation and migration. These processes might be regulated by PPAR-γ signaling pathway.

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敲除 AMIGO2 可通过调节 PPAR-γ 抑制膀胱癌的增殖和迁移。

目的：本研究旨在揭示AMIGO2与膀胱癌的增殖、迁移和致瘤性之间的关系，并探讨其潜在的分子机制：方法：通过qRT-PCR和免疫组织化学（IHC）检测AMIGO2的表达水平。通过慢病毒转染建立稳定的 AMIGO2 基因敲除细胞系 T24 和 5637。利用细胞计数试剂盒（CCK-8 检测法）测定细胞增殖，利用流式细胞仪分析检测细胞周期，并进行伤口愈合试验测试膀胱癌细胞的迁移能力。建立了异种移植小鼠模型，以研究 AMIGO2 对体内肿瘤形成的影响。应用 RNA 测序技术探索其潜在机制。结果表明：AMIGO2在膀胱癌细胞中上调：结果：AMIGO2在膀胱癌细胞和组织中上调。抑制 AMIGO2 的表达可抑制细胞的增殖和迁移。AMIGO2的低表达抑制了裸鼠5637的致瘤性。根据RNA-Seq和生物信息学分析，确定了917个DEGs。这些DEGs主要富集在细胞-细胞粘附、过氧化物酶体增殖激活受体（PPARs）信号通路和其他一些通路中。PPAR-γ在膀胱癌细胞株T24和5637中高表达，但当AMIGO2在T24和5637中被敲除时，PPAR-γ的表达水平也会下降，PPAR-γ的过表达可以逆转抑制AMIGO2对细胞增殖和迁移的抑制作用：结论：AMIGO2在膀胱癌细胞和组织中过表达。结论：AMIGO2在膀胱癌细胞和组织中过表达，敲除AMIGO2可抑制膀胱癌细胞的增殖和迁移。这些过程可能受 PPAR-γ 信号通路调控。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Hereditas Biochemistry, Genetics and Molecular Biology-Genetics

CiteScore

3.80

自引率

3.70%

发文量

期刊介绍： For almost a century, Hereditas has published original cutting-edge research and reviews. As the Official journal of the Mendelian Society of Lund, the journal welcomes research from across all areas of genetics and genomics. Topics of interest include human and medical genetics, animal and plant genetics, microbial genetics, agriculture and bioinformatics.