LINC00857 promotes cell proliferation and migration in colorectal cancer by interacting with YTHDC1 and stabilizing SLC7A5
Affiliations: Department of Internal Medicine‑Oncology, Chenzhou No. 1 People's Hospital, Chenzhou, Hunan 423000, P.R. China, Hospital Medical Department, Chenzhou No. 1 People's Hospital, Chenzhou, Hunan 423000, P.R. China, Department of Gastrointestinal Surgery, Chenzhou No. 1 People's Hospital, Chenzhou, Hunan 423000, P.R. China
- Published online on: June 2, 2021 https://doi.org/10.3892/ol.2021.12839
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Colorectal cancer (CRC) is one of the most lethal malignances in humans. Hence, it is of great significance to identify regulatory molecules in CRC progression. Accumulating evidence has demonstrated that long non‑coding RNAs (lncRNAs) are involved in cancer malignancy. It has been reported that long intergenic non‑protein coding RNA 857 (LINC00857) acts as a vital oncogene in many types of cancer by promoting cell proliferation and migration. However, the role of LINC00857 in CRC remains unclear. In the present study, LINC00857 was upregulated in CRC tissue samples and cells. Next, in vitro loss‑of‑function experiments demonstrated that LINC00857 knockdown suppressed CRC cell viability, proliferation and migration, as well as epithelial‑mesenchymal transition and increased cell apoptosis. Mechanistically, LINC00857 abundantly interacted with the RNA‑binding protein YTH domain containing 1 (YTHDC1). YTHDC1 ultimately combined with solute carrier family 7 member 5 (SLC7A5) and increased SLC7A5 mRNA stability. Finally, a series of rescue experiments indicated that LINC00857 promoted the proliferation and migration of CRC cells by regulating mRNA stability. Thus, the present findings illustrated that LINC00857 functions as an oncogene in CRC cells via the YTHDC1/SLC7A5 axis.