Full text

Turn on search term navigation

© 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.

Abstract

The WNT1 inducible signaling pathway protein 1 (WISP1), a member of the connective tissue growth factor family, plays a crucial role in several important cellular functions in a highly tissue-specific manner. Results of a RT-qPCR indicated that WISP1 expressed only in cells of the human prostate fibroblasts, HPrF and WPMY-1, but not the prostate carcinoma cells in vitro. Two major isoforms (WISP1v1 and WISP1v2) were identified in the HPrF cells determined by RT-PCR and immunoblot assays. The knock-down of a WISP1 blocked cell proliferation and contraction, while treating respectively with the conditioned medium from the ectopic WISP1v1- and WISPv2-overexpressed 293T cells enhanced the migration of HPrF cells. The TNFα induced WISP1 secretion and cell contraction while the knock-down of WISP1 attenuated these effects, although TNFα did not affect the proliferation of the HPrF cells. The ectopic overexpression of WISP1v1 but not WISP1v2 downregulated the N-myc downstream regulated 1 (NDRG1) while upregulating N-cadherin, slug, snail, and vimentin gene expressions which induced not only the cell proliferation and invasion in vitro but also tumor growth of prostate carcinoma cells in vivo. The results confirmed that WISP1 is a stroma-specific secreting protein, enhancing the cell migration and contraction of prostate fibroblasts, as well as the proliferation, invasion, and tumor growth of prostate carcinoma cells.

Details

Title
WNT1 Inducible Signaling Pathway Protein 1 Is a Stroma-Specific Secreting Protein Inducing a Fibroblast Contraction and Carcinoma Cell Growth in the Human Prostate
Author
Kang-Shuo Chang 1 ; Chen, Syue-Ting 2 ; Hsin-Ching, Sung 3 ; Shu-Yuan, Hsu 3 ; Wei-Yin, Lin 4 ; Chen-Pang, Hou 5 ; Yu-Hsiang, Lin 5   VIAFID ORCID Logo  ; Tsui-Hsia, Feng 6 ; Ke-Hung Tsui 7   VIAFID ORCID Logo  ; Horng-Heng Juang 2   VIAFID ORCID Logo 

 Department of Anatomy, College of Medicine, Chang Gung University, Kwei-Shan, Taoyuan 33302, Taiwan 
 Department of Anatomy, College of Medicine, Chang Gung University, Kwei-Shan, Taoyuan 33302, Taiwan; Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Kwei-Shan, Taoyuan 33302, Taiwan; Department of Urology, Chang Gung Memorial Hospital-Linkou, Kwei-Shan, Taoyuan 33302, Taiwan 
 Department of Anatomy, College of Medicine, Chang Gung University, Kwei-Shan, Taoyuan 33302, Taiwan; Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Kwei-Shan, Taoyuan 33302, Taiwan 
 Department of Internal Medicine, Chang Gung Memorial Hospital-Linkou, Kwei-Shan, Taoyuan 33302, Taiwan 
 Department of Urology, Chang Gung Memorial Hospital-Linkou, Kwei-Shan, Taoyuan 33302, Taiwan 
 School of Nursing, College of Medicine, Chang Gung University, Kwei-Shan, Taoyuan 33302, Taiwan 
 Department of Urology, Shuang Ho Hospital, New Taipei City 235041, Taiwan; TMU Research Center of Urology and Kidney, Department of Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan 
First page
11437
Publication year
2022
Publication date
2022
Publisher
MDPI AG
ISSN
16616596
e-ISSN
14220067
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2724286058
Copyright
© 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.