Journal
CELL BIOLOGY INTERNATIONAL
Volume 45, Issue 2, Pages 368-381Publisher
WILEY
DOI: 10.1002/cbin.11493
Keywords
5‐ FU; colorectal cancer; EMT; invasion; MARCH1; migration
Categories
Funding
- Shandong Province Traditional Chinese Medicine Technology Development Plan of Chian [2019-0517]
- Shandong Province Key R&D Program (Public Welfare) of China [2019GSF107099]
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The study found that MARCH1 is highly expressed in colorectal cancer and its regulation of epithelial-mesenchymal transition and the PI3K/AKT pathway affects tumor cell migration and invasion. 5-fluorouracil targets MARCH1 and downregulates the PI3K/AKT pathway, inhibiting proliferation, migration, and invasion of tumor cells.
Colorectal cancer is a major health problem with a significant impact on the patients' quality of life. 5-Fluorouracil is the most common chemotherapy drug used for this type of cancer. While its molecular mechanism is the inhibition of DNA synthesis via the inhibition of thymine nucleotide synthetase, its complete anticancer mechanism is not clear. Membrane-associated RING-CH-1 (MARCH1) is an E3 ubiquitin ligase that plays an important role in antigen presentation. However, MARCH1 has not been studied in the context of colorectal cancer. In this study, we demonstrated that MARCH1 is highly expressed in colorectal cancer tissues and cell lines. Furthermore, migration and invasion of colorectal tumor cells were inhibited via transfection with small interfering RNAs to suppress the expression of MARCH1. The western blot analysis showed that MARCH1 regulates epithelial-mesenchymal transition and the PI3K/AKT pathway. Moreover, 5-fluorouracil inhibited the proliferation, migration, and invasion of tumor cells, via the targeting of MARCH1 and the consequent downregulation of the PI3K/AKT pathway, impacting the progression of epithelial-mesenchymal transition. In conclusion, our study shows that MARCH1 may play a role as an oncogene in colorectal cancer and may represent a new target molecule of 5-fluorouracil.
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