TY - JOUR
T1 - Epithelial–mesenchymal plasticity in cancer
T2 - signaling pathways and therapeutic targets
AU - Wang, Xiangpeng
AU - Xue, Xiaoxia
AU - Pang, Mingshi
AU - Yu, Liuchunyang
AU - Qian, Jinxiu
AU - Li, Xiaoyu
AU - Tian, Meng
AU - Lyu, Aiping
AU - Lu, Cheng
AU - Liu, Yuanyan
N1 - Funding Information:
Special thanks for the long-term subsidy mechanism from the Ministry of Finance and the Ministry of Education of PRC (People's Republic of China) for BUCM (Beijing University of Chinese Medicine). This work was supported by the Innovation Team and Talents Cultivation Program of National Administration of Traditional Chinese Medicine. (No: ZYYCXTD-D-202005) and the Youth Qihuang Scholar of National Administration of Traditional Chinese Medicine (2020).
Publisher Copyright:
© 2024 The Author(s). MedComm published by Sichuan International Medical Exchange & Promotion Association (SCIMEA) and John Wiley & Sons Australia, Ltd.
PY - 2024/8
Y1 - 2024/8
N2 - Currently, cancer is still a leading cause of human death globally. Tumor deterioration comprises multiple events including metastasis, therapeutic resistance and immune evasion, all of which are tightly related to the phenotypic plasticity especially epithelial–mesenchymal plasticity (EMP). Tumor cells with EMP are manifest in three states as epithelial–mesenchymal transition (EMT), partial EMT, and mesenchymal–epithelial transition, which orchestrate the phenotypic switch and heterogeneity of tumor cells via transcriptional regulation and a series of signaling pathways, including transforming growth factor-β, Wnt/β-catenin, and Notch. However, due to the complicated nature of EMP, the diverse process of EMP is still not fully understood. In this review, we systematically conclude the biological background, regulating mechanisms of EMP as well as the role of EMP in therapy response. We also summarize a range of small molecule inhibitors, immune-related therapeutic approaches, and combination therapies that have been developed to target EMP for the outstanding role of EMP-driven tumor deterioration. Additionally, we explore the potential technique for EMP-based tumor mechanistic investigation and therapeutic research, which may burst vigorous prospects. Overall, we elucidate the multifaceted aspects of EMP in tumor progression and suggest a promising direction of cancer treatment based on targeting EMP.
AB - Currently, cancer is still a leading cause of human death globally. Tumor deterioration comprises multiple events including metastasis, therapeutic resistance and immune evasion, all of which are tightly related to the phenotypic plasticity especially epithelial–mesenchymal plasticity (EMP). Tumor cells with EMP are manifest in three states as epithelial–mesenchymal transition (EMT), partial EMT, and mesenchymal–epithelial transition, which orchestrate the phenotypic switch and heterogeneity of tumor cells via transcriptional regulation and a series of signaling pathways, including transforming growth factor-β, Wnt/β-catenin, and Notch. However, due to the complicated nature of EMP, the diverse process of EMP is still not fully understood. In this review, we systematically conclude the biological background, regulating mechanisms of EMP as well as the role of EMP in therapy response. We also summarize a range of small molecule inhibitors, immune-related therapeutic approaches, and combination therapies that have been developed to target EMP for the outstanding role of EMP-driven tumor deterioration. Additionally, we explore the potential technique for EMP-based tumor mechanistic investigation and therapeutic research, which may burst vigorous prospects. Overall, we elucidate the multifaceted aspects of EMP in tumor progression and suggest a promising direction of cancer treatment based on targeting EMP.
KW - cancer
KW - cell plasticity
KW - deterioration
KW - EMT
KW - signaling pathway
UR - http://www.scopus.com/inward/record.url?scp=85200130665&partnerID=8YFLogxK
U2 - 10.1002/mco2.659
DO - 10.1002/mco2.659
M3 - Review article
AN - SCOPUS:85200130665
SN - 2688-2663
VL - 5
JO - MedComm
JF - MedComm
IS - 8
M1 - e659
ER -