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Research Paper|Volume 11, Issue 18|pp 7914—7937

TIP-B1 promotes kidney clear cell carcinoma growth and metastasis via EGFR/AKT signaling

Lei Yin1, Shenglin Gao2, Heng Shi1,3, Keyi Wang1, Huan Yang4, Bo Peng1
  • 1Department of Urology, Shanghai Tenth People’s Hospital, School of Medicine in Tongji University, Shanghai, China
  • 2Department of Urology, Changzhou No. 2 People’s Hospital, Nanjing Medical University, Changzhou, Jiangsu, China
  • 3Department of Urology, Shanghai Tenth People’s Hospital, Nanjing Medical University, Nanjing, China
  • 4Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
Received: August 9, 2019Accepted: September 14, 2019Published: September 27, 2019
https://doi.org/10.18632/aging.102298

Copyright © 2019 Yin et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Kidney clear cell carcinoma (KIRC) is the most prevalent kidney malignancy. Accumulating evidence shows that high expression of TIP-B1 correlates with development of tumor progression. However, the detailed functions of TIP-B1 in the KIRC remain to be further elucidated. Here, we firstly found TIP-B1 expression was significantly increased in KIRC compared with adjacent normal tissues. What’s more, higher expression of TIP-B1 were correlated with aggressive clinico-pathological characteristics. In vitro assay found TIP-B1 knockdown dramatically inhibited KIRC cells proliferation, migration and invasion. In vivo assay found down regulated TIP-B1 could suppress tumor growth and metastasis. Mechanism analysis indicated that TIP-B1 could bind EGFR and suppress EGFR degradation, then promoted EGF-induced AKT signaling. Together, TIP-B1 could be applied as an independent risk factor to predict KIRC progression and metastasis. Targeting TIP-B1 might be a new potential therapeutic strategy for KIRC treatment.