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TRIB3 通过激活 MAPK 信号通路促进肾细胞癌细胞的增殖和侵袭。

TRIB3 Promotes the Proliferation and Invasion of Renal Cell Carcinoma Cells via Activating MAPK Signaling Pathway.

机构信息

Department of Urology, Peking University First Hospital, Beijing 100034, P.R. China.

Hereditary Kidney Cancer Research Center, Peking University First Hospital, Beijing 100034, P.R. China.

出版信息

Int J Biol Sci. 2019 Jan 1;15(3):587-597. doi: 10.7150/ijbs.29737. eCollection 2019.

Abstract

Tribbles pseudokinase 3 (TRIB3) is a member of the mammalian pseudokinase tribbles family and is involved in multiple biological processes. However, the role of TRIB3 in renal cell carcinoma (RCC) remains unclear. In this study, we aimed to elucidate the biological functions of TRIB3 in RCC and explore its underlying mechanisms. TRIB3 expression and its correlation with clinicopathological features was evaluated in 123 patients with RCC. A series of cytological experiments were performed to clarify the biological functions of TRIB3, and potential molecular regulatory mechanisms were explored using transcriptome sequencing. TRIB3 expression was significantly elevated in RCC tissues compared to that in paracancerous tissues, and high expression of TRIB3 was correlated with both advanced tumor stage and unfavorable prognosis. TRIB3 knockdown markedly inhibited RCC cell proliferation, migration and invasion. Furthermore, overexpression of TRIB3 promoted RCC cell proliferation, migration, invasion and xenograft tumor growth. Notably, TRIB3 expression was modulated by hypoxia-inducible factor-1α (HIF-1α), which enhanced cell viability and invasiveness via targeting the MAPK signaling pathway. This study reveals the potential oncogenic role of TRIB3 in RCC pathogenesis and illustrates the mechanisms underlying TRIB3-mediated tumor progression, providing new insight into the development of TRIB3 as a tumor biomarker and therapeutic target.

摘要

TRIB3 是哺乳动物 tribbles 家族的一员,涉及多种生物学过程。然而,TRIB3 在肾细胞癌(RCC)中的作用尚不清楚。在这项研究中,我们旨在阐明 TRIB3 在 RCC 中的生物学功能,并探讨其潜在的机制。评估了 123 例 RCC 患者的 TRIB3 表达及其与临床病理特征的相关性。进行了一系列细胞学实验以阐明 TRIB3 的生物学功能,并通过转录组测序探讨潜在的分子调控机制。与癌旁组织相比,TRIB3 在 RCC 组织中的表达明显升高,且 TRIB3 高表达与肿瘤分期较晚和预后不良相关。TRIB3 敲低显著抑制 RCC 细胞的增殖、迁移和侵袭。此外,TRIB3 的过表达促进了 RCC 细胞的增殖、迁移、侵袭和异种移植肿瘤的生长。值得注意的是,TRIB3 的表达受缺氧诱导因子-1α(HIF-1α)调节,通过靶向 MAPK 信号通路增强细胞活力和侵袭性。本研究揭示了 TRIB3 在 RCC 发病机制中的潜在致癌作用,并阐明了 TRIB3 介导的肿瘤进展的机制,为 TRIB3 作为肿瘤标志物和治疗靶点的发展提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd52/6367588/3969884107d8/ijbsv15p0587g001.jpg

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