Overview and new insights of lysine-specific histone demethylase 1 in colorectal cancer: promoting epithelial-mesenchymal transition and stemness features of cancer stem cells
Author:
Chen Jiang1ORCID, Yang Tao1, Xiao Tianbao1, Wang Ziwei2, He Fan3, Bao Tian-tian1, Cao Yibo1
Affiliation:
1. Department of Anorectal Surgery , 586762 The First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine , Guiyang , Guizhou , China 2. Department of Gastrointestinal Surgery , 117972 The First Affiliated Hospital of Chongqing Medical University , Chongqing , China 3. Department of Oncology , 586762 The First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine , Guiyang , Guizhou , China
Abstract
Abstract
Colorectal cancer (CRC) is a common malignant tumor, and research on its pathological mechanism has received increasing attention. Most CRC patients have a poor prognosis, and there is still a lack of effective immunotherapy options. An in-depth exploration of the molecular mechanism of CRC occurrence and development is of great clinical significance for the diagnosis, treatment guidance, and prognosis of CRC. Lysine-specific histone demethylase 1 (LSD1) is highly expressed in CRC, and closely related to the occurrence, invasion, metastasis, and drug resistance of CRC. The histone H3K27 demethylase KDM6A forms an inhibitory complex with LSD1 and other epigenetic regulators, silencing epithelial-mesenchymal transition (EMT) transcription factors and inhibiting EMT-induced cancer stem cells (CSCs) properties. LSD1 is a promising target for CRC therapy, some LSD1 inhibitors are in the experimental stage by blocking its demethylase activity and may benefit CRC patients in the clinical treatment course in the future. This article reviews the latest research progress on the function of LSD1 and its relationship with CRC.
Funder
Science and Technology Project of Guizhou Province PhD start-up fund of the First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine
Publisher
Walter de Gruyter GmbH
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