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MCC in the spotlight: Its dual role in signal regulation and oncogenesis
Soohyeon Lee1, Beomwoo Lee1, So Hee Kwon2
1Department of Pharmacology, College of Medicine, Chungnam National University, Daejeon 35015, South Korea; Department of Medical Science, Metabolic Syndrome and Cell Signaling Laboratory, Institute for Cancer Research, College of Medicine, Chungnam National University, Daejeon 35015, South Korea.
Abstract:
The mutated in colorectal cancer (MCC) gene is closely associated with the onset and progression of colorectal cancer. MCC plays a critical role in regulating the cell cycle and various signaling pathways and is recognized to inhibit cancer cell proliferation via the β-catenin signaling pathway. β-catenin is a key component of the WNT signaling pathway that influences cell growth, differentiation, survival, and migration, thereby positioning MCC as an important tumor suppressor. Notably, MCC has also been implicated in other cancer types, including lung, liver, and brain cancers. However, the precise mechanisms by which MCC functions in these malignancies remain inadequately understood. Comprehensive investigations into the interactions among MCC, various signaling pathways, and metabolic processes are essential for uncovering the molecular mechanisms of cancer and the pathological features characteristic of different cancer stages. This review presents the structural characteristics of MCC and its cell growth regulation mechanisms and functional roles within tissues, with the aims of enhancing our understanding of the role of MCC in cancer biology and highlighting potential therapeutic strategies targeting this gene.
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