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Loss of Rab25 promotes the development of skin squamous cell carcinoma through the dysregulation of integrin trafficking

Authors
 Haengdueng Jeong  ;  Kyung‐Min Lim  ;  Kwang H Kim  ;  Yejin Cho  ;  Buhyun Lee  ;  Byron C Knowles  ;  Joseph T Roland  ;  Jeffrey P Zwerner  ;  James R Goldenring  ;  Ki Taek Nam 
Citation
 Journal of Pathology, Vol.249(2) : 227-240, 2019 
Journal Title
 Journal of Pathology 
ISSN
 0022-3417 
Issue Date
2019
Keywords
Rab25 ; epidermis ; integrin ; skin ; squamous cell carcinoma (SCC)
Abstract
Rab25 can function as both a tumor suppressor and a tumor promoter across different tissues. This study sought to clarify the role of Rab25 as a tumor suppressor in skin squamous cell carcinoma (SCC). Rab25 loss was closely associated with neoplastic transition in both humans and mice. Rab25 loss was well correlated with increased cell proliferation and poor differentiation in human SCC. While Rab25 knockout (KO) in mice did not induce spontaneous tumor formation, it did significantly accelerate tumor generation and promote malignant transformation in a mouse two-stage skin carcinogenesis model. Xenografting of a Rab25-deficient human keratinocyte cell line, HaCaT, also elicited neoplastic transformation. Notably, Rab25 deficiency led to dysregulation of integrins β1, β4, and α6, which matched well with increased epidermal proliferation and impaired desmosome-tight junction formation. Rab25 deficiency induced impairment of integrin recycling, leading to the improper expression of integrins. In line with this, significant attenuation of integrin β1, β4, and α6 expression was identified in human SCCs where Rab25 was deficient. Collectively, these results suggest that loss of Rab25 promotes the development and neoplastic transition of SCC through dysregulation of integrin trafficking. © 2019 Pathological Society of Great Britain and Ireland.
Full Text
https://onlinelibrary.wiley.com/doi/full/10.1002/path.5311
DOI
10.1002/path.5311
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Nam, Ki Taek(남기택)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/171463
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