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Cell metabolism

Cell metabolism

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The diapause-like colorectal cancer cells induced by SMC4 attenuation are characterized by low proliferation and chemotherapy insensitivity.

Published:5 September 2023 DOI: 10.1016/j.cmet.2023.07.005 PMID: 37543034
Xuedan Sun, Lifang He, Hong Liu, Rick Francis Thorne, Taofei Zeng, Liu Liu, Bo Zhang, Miao He, Yabin Huang, Mingyue Li, Enyi Gao, Mengyao Ma, Cheng Cheng, Fanzheng Meng, Chuandong Lang, Hairui Li, Wanxiang Xiong, Shixiang Pan, Delong Ren, Bingyi Dang, Yi Yang, Mian Wu, Lianxin Liu

Abstract

In response to adverse environmental conditions, embryonic development may reversibly cease, a process termed diapause. Recent reports connect this phenomenon with the non-genetic responses of tumors to chemotherapy, but the mechanisms involved are poorly understood. Here, we establish a multifarious role for SMC4 in the switching of colorectal cancer cells to a diapause-like state. SMC4 attenuation promotes the expression of three investment phase glycolysis enzymes increasing lactate production while also suppressing PGAM1. Resultant high lactate levels increase ABC transporter expression via histone lactylation, rendering tumor cells insensitive to chemotherapy. SMC4 acts as co-activator of PGAM1 transcription, and the coordinate loss of SMC4 and PGAM1 affects F-actin assembly, inducing cytokinesis failure and polyploidy, thereby inhibiting cell proliferation. These insights into the mechanisms underlying non-genetic chemotherapy resistance may have significant implications for the field, advancing our understanding of aerobic glycolysis functions in tumor and potentially informing future therapeutic strategies.

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