RASAL2 inhibits tumor angiogenesis via p-AKT/ETS1 signaling in bladder cancer

Ke Hui, Shiqi Wu, Yangyang Yue, Yanan Gu, Bing Guan, Xinyang Wang, Jer Tsong Hsieh, Luke S. Chang, Dalin He, Kaijie Wu

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Muscle-invasive or metastatic bladder cancer (BCa) is a life-threatening disease for patients, and tumor angiogenesis is believed to play a critical role in the progression of BCa. However, its underlying mechanism of tumor angiogenesis is still poorly understood. In this study, we discovered that RASAL2, a RAS GTPase activating protein, could inhibit BCa angiogenesis based on our shRNA/siRNA knockdown or ectopic cDNA expression experiments. Mechanistically, RASAL2 downregulation could enhance the phosphorylation of AKT and then subsequently upregulate the expression of ETS1 and VEGFA. Furthermore, there was a negative correlation between RASAL2 and VEGFA or CD31 expression in subcutaneous xenograft and human BCa specimens. Taken together, we provide a new insight into the molecular mechanism of BCa progression, in which RASAL2 can be a new therapeutic target.

Original languageEnglish (US)
Pages (from-to)38-44
Number of pages7
JournalCellular Signalling
Volume48
DOIs
StatePublished - Aug 1 2018

Fingerprint

Urinary Bladder Neoplasms
Neoplasms
Small Interfering RNA
GTPase-Activating Proteins
Heterografts
Up-Regulation
Down-Regulation
Complementary DNA
Phosphorylation
Muscles
Therapeutics

Keywords

  • AKT/ETS1 signaling
  • Angiogenesis
  • Bladder cancer
  • RASAL2
  • VEGFA

ASJC Scopus subject areas

  • Cell Biology

Cite this

RASAL2 inhibits tumor angiogenesis via p-AKT/ETS1 signaling in bladder cancer. / Hui, Ke; Wu, Shiqi; Yue, Yangyang; Gu, Yanan; Guan, Bing; Wang, Xinyang; Hsieh, Jer Tsong; Chang, Luke S.; He, Dalin; Wu, Kaijie.

In: Cellular Signalling, Vol. 48, 01.08.2018, p. 38-44.

Research output: Contribution to journalArticle

Hui, K, Wu, S, Yue, Y, Gu, Y, Guan, B, Wang, X, Hsieh, JT, Chang, LS, He, D & Wu, K 2018, 'RASAL2 inhibits tumor angiogenesis via p-AKT/ETS1 signaling in bladder cancer', Cellular Signalling, vol. 48, pp. 38-44. https://doi.org/10.1016/j.cellsig.2018.04.006
Hui, Ke ; Wu, Shiqi ; Yue, Yangyang ; Gu, Yanan ; Guan, Bing ; Wang, Xinyang ; Hsieh, Jer Tsong ; Chang, Luke S. ; He, Dalin ; Wu, Kaijie. / RASAL2 inhibits tumor angiogenesis via p-AKT/ETS1 signaling in bladder cancer. In: Cellular Signalling. 2018 ; Vol. 48. pp. 38-44.
@article{055b09e6bc4a4bc3845e5d8eaf7787d7,
title = "RASAL2 inhibits tumor angiogenesis via p-AKT/ETS1 signaling in bladder cancer",
abstract = "Muscle-invasive or metastatic bladder cancer (BCa) is a life-threatening disease for patients, and tumor angiogenesis is believed to play a critical role in the progression of BCa. However, its underlying mechanism of tumor angiogenesis is still poorly understood. In this study, we discovered that RASAL2, a RAS GTPase activating protein, could inhibit BCa angiogenesis based on our shRNA/siRNA knockdown or ectopic cDNA expression experiments. Mechanistically, RASAL2 downregulation could enhance the phosphorylation of AKT and then subsequently upregulate the expression of ETS1 and VEGFA. Furthermore, there was a negative correlation between RASAL2 and VEGFA or CD31 expression in subcutaneous xenograft and human BCa specimens. Taken together, we provide a new insight into the molecular mechanism of BCa progression, in which RASAL2 can be a new therapeutic target.",
keywords = "AKT/ETS1 signaling, Angiogenesis, Bladder cancer, RASAL2, VEGFA",
author = "Ke Hui and Shiqi Wu and Yangyang Yue and Yanan Gu and Bing Guan and Xinyang Wang and Hsieh, {Jer Tsong} and Chang, {Luke S.} and Dalin He and Kaijie Wu",
year = "2018",
month = "8",
day = "1",
doi = "10.1016/j.cellsig.2018.04.006",
language = "English (US)",
volume = "48",
pages = "38--44",
journal = "Cellular Signalling",
issn = "0898-6568",
publisher = "Elsevier Inc.",

}

TY - JOUR

T1 - RASAL2 inhibits tumor angiogenesis via p-AKT/ETS1 signaling in bladder cancer

AU - Hui, Ke

AU - Wu, Shiqi

AU - Yue, Yangyang

AU - Gu, Yanan

AU - Guan, Bing

AU - Wang, Xinyang

AU - Hsieh, Jer Tsong

AU - Chang, Luke S.

AU - He, Dalin

AU - Wu, Kaijie

PY - 2018/8/1

Y1 - 2018/8/1

N2 - Muscle-invasive or metastatic bladder cancer (BCa) is a life-threatening disease for patients, and tumor angiogenesis is believed to play a critical role in the progression of BCa. However, its underlying mechanism of tumor angiogenesis is still poorly understood. In this study, we discovered that RASAL2, a RAS GTPase activating protein, could inhibit BCa angiogenesis based on our shRNA/siRNA knockdown or ectopic cDNA expression experiments. Mechanistically, RASAL2 downregulation could enhance the phosphorylation of AKT and then subsequently upregulate the expression of ETS1 and VEGFA. Furthermore, there was a negative correlation between RASAL2 and VEGFA or CD31 expression in subcutaneous xenograft and human BCa specimens. Taken together, we provide a new insight into the molecular mechanism of BCa progression, in which RASAL2 can be a new therapeutic target.

AB - Muscle-invasive or metastatic bladder cancer (BCa) is a life-threatening disease for patients, and tumor angiogenesis is believed to play a critical role in the progression of BCa. However, its underlying mechanism of tumor angiogenesis is still poorly understood. In this study, we discovered that RASAL2, a RAS GTPase activating protein, could inhibit BCa angiogenesis based on our shRNA/siRNA knockdown or ectopic cDNA expression experiments. Mechanistically, RASAL2 downregulation could enhance the phosphorylation of AKT and then subsequently upregulate the expression of ETS1 and VEGFA. Furthermore, there was a negative correlation between RASAL2 and VEGFA or CD31 expression in subcutaneous xenograft and human BCa specimens. Taken together, we provide a new insight into the molecular mechanism of BCa progression, in which RASAL2 can be a new therapeutic target.

KW - AKT/ETS1 signaling

KW - Angiogenesis

KW - Bladder cancer

KW - RASAL2

KW - VEGFA

UR - http://www.scopus.com/inward/record.url?scp=85046171518&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85046171518&partnerID=8YFLogxK

U2 - 10.1016/j.cellsig.2018.04.006

DO - 10.1016/j.cellsig.2018.04.006

M3 - Article

VL - 48

SP - 38

EP - 44

JO - Cellular Signalling

JF - Cellular Signalling

SN - 0898-6568

ER -