CD271 promotes proliferation and migration in bladder cancer

Author:

Myoen Shingo123,Mochizuki Mai1,Shibuya‐Takahashi Rie1,Fujimori Haruna1,Shindo Norihisa4,Yamaguchi Kazunori4,Yasuda Jun4,Abe Jiro5,Imai Takayuki6,Sato Ikuro7,Adachi Hisanobu2,Kawamura Sadafumi2,Ito Akihiro3,Tamai Keiichi1ORCID

Affiliation:

1. Division of Cancer Stem Cell Miyagi Cancer Center Research Institute Natori Miyagi Japan

2. Division of Urology Miyagi Cancer Center Natori Miyagi Japan

3. Department of Urology Tohoku University Graduate School of Medicine Sendai Miyagi Japan

4. Division of Molecular and Cellular Oncology Miyagi Cancer Center Research Institute Natori Miyagi Japan

5. Division of Thoracic Surgery Miyagi Cancer Center Natori Miyagi Japan

6. Division of Head and Neck Surgery Miyagi Cancer Center Natori Miyagi Japan

7. Division of Pathology Miyagi Cancer Center Natori Miyagi Japan

Abstract

AbstractBladder cancer is a urothelial cancer and effective therapeutic strategies for its advanced stages are limited. Here, we report that CD271, a neurotrophin receptor, promotes the proliferation and migration of bladder cancer cells. CD271 knockdown decreased proliferation in both adherent and spheroid cultures, and vice versa when CD271 was overexpressed in bladder cancer cell lines. CD271 depletion impaired tumorigenicity in vivo. Migration activity was reduced by CD271 knockdown and TAT‐Pep5, a known CD271‐Rho GDI‐binding inhibitor. Apoptosis was induced by CD271 knockdown. Comprehensive gene expression analysis revealed alterations in E2F‐ and Myc‐related pathways upon CD271 expression. In clinical cases, patients with high CD271 expression showed significantly shortened overall survival. In surgically resected specimens, pERK, a known player in proliferation signaling, colocalizes with CD271. These data indicate that CD271 is involved in bladder cancer malignancy by promoting cell proliferation and migration, resulting in poor prognosis.

Funder

Japan Society for the Promotion of Science

Publisher

Wiley

Subject

Cell Biology,Genetics

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