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Copyright (c) 2025 Shizhuan Huang, Zhizhou Li, Haotian Wu, Daowei Tang, Zhanyi Xiao, Yongji Liu, Xiaowei Jing, Sheng Tai, Guanqun Liao
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.MORC2 facilitates cholangiocarcinoma progression through cell cycle acceleration and immune microenvironment modification
Corresponding Author(s) : Shizhuan Huang
Cellular and Molecular Biology,
Vol. 71 No. 4: Issue 4
Abstract
This study explored a novel therapeutic target, MORC2 (Microrchidia family CW-type zinc finger 2), for patients with unresectable advanced Cholangiocarcinoma (CCA), a lethal epithelial cell malignancy lacking effective treatments. Utilizing bioinformatics analysis, we examined MORC2's role in CCA progression. The focus was on its association with the cell cycle and its involvement in the tumor's immunosuppressive microenvironment. MORC2 was found to accelerate CCA cell proliferation by promoting cell cycle progression through the activation of TNF-α signaling via the NFKB signaling pathway. Furthermore, the downregulation of MORC2 induced cell cycle arrest and might facilitate neutrophil infiltration by upregulating CCL3, indicating its pivotal role in modifying the immunosuppressive tumor microenvironment. Our findings suggest that MORC2 plays a crucial role in both the proliferation of CCA cells and the modification of the tumor microenvironment. Targeting MORC2 presents a novel potential therapeutic approach for patients with advanced CCA.
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