Molecular mechanisms of tumour budding and its association with microenvironment in colorectal cancer

被引:6
作者
Hatthakarnkul, Phimmada [1 ]
Quinn, Jean A. [1 ]
Ammar, Aula [1 ]
Lynch, Gerard [1 ]
Van Wyk, Hester [2 ]
McMillan, Donald C. [2 ]
Thuwajit, Chanitra [3 ]
Edwards, Joanne [1 ]
机构
[1] Univ Glasgow, Wolfson Wohl Canc Res Ctr, Inst Canc Sci, Glasgow G61 1QH, Lanark, Scotland
[2] Univ Glasgow, Glasgow Royal Infirm, Sch Med, Glasgow G31 2ER, Lanark, Scotland
[3] Mahidol Univ, Fac Med, Dept Immunol, Siriraj Hosp, Bangkok 10700, Thailand
关键词
EPITHELIAL-MESENCHYMAL TRANSITION; STEM-CELLS; EXPRESSION; SURVIVAL; EMT; HETEROGENEITY; INFILTRATION; RESISTANCE; BIOMARKERS; PHENOTYPE;
D O I
10.1042/CS20210886
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Colorectal cancer (CRC) is the third most common cancer worldwide. Poor survival of CRC associated with the development of tumour metastasis led to the investigation of the potential biomarkers to predict outcomes in CRC patients. Tumour budding (TB) is a well-known independent prognostic marker for poor survival and disease metastasis. Therefore, it has been suggested that TB status is included in routine clinicopathological factors for risk assessment in CRC. In contrast with a vast majority of studies regarding the prognostic power of TB, there is no clear evidence pertaining to the underlying molecular mechanism driving this phenotype, or an understanding of TB relationship with the tumour microenvironment (TME). The aim of the present study is to present a comprehensive review of TB and tumour cell signalling pathways together with the cross-talk of immune cells that could drive TB formation in CRC.
引用
收藏
页码:521 / 535
页数:15
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