Abstract
This study investigates the role of the long non-coding RNA EGOT in colorectal cancer (CRC) by examining its expression in 40 pairs of CRC and adjacent normal tissues and assessing its impact on clinical outcomes. EGOT was found to be downregulated in CRC tissues, and low EGOT levels were associated with a higher likelihood of lymphatic and distant metastasis, as well as poorer overall and progression-free survival in CRC patients. Functional experiments revealed that overexpression of EGOT in SW480 cells reduced cell viability, migration, and wound closure, while knockdown of EGOT in LoVo cells had the opposite effect. In vivo experiments with nude mice confirmed that EGOT downregulation accelerated CRC growth, whereas its overexpression slowed tumor growth. The study identified BTG3 as the target gene of EGOT, and they exhibited a negative correlation in CRC tissues. Rescue experiments demonstrated that BTG3 could reverse the effects of EGOT on CRC cell phenotypes. In conclusion, EGOT is a downregulated molecule in CRC, closely associated with metastasis and patient prognosis. It exerts a suppressive influence on CRC cell proliferation, migration, and tumorigenesis by negatively regulating BTG3.
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