miR‑590‑5p may regulate colorectal cancer cell viability and migration by targeting PDCD4
- Ting Guo
- Jun Wang
- Guochang Cheng
- He Huang
Affiliations: Central Laboratory, Taizhou People's Hospital, Taizhou, Jiangsu 225300, P.R. China, Department of Emergency, Taizhou People's Hospital, Taizhou, Jiangsu 225300, P.R. China, Department of Surgery, Taizhou People's Hospital, Taizhou, Jiangsu 225300, P.R. China, Department of Oncology, Taizhou People's Hospital, Taizhou, Jiangsu 225300, P.R. China
- Published online on: September 4, 2020 https://doi.org/10.3892/etm.2020.9183
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Recent studies have revealed that microRNAs (miRs) are involved in the pathogenesis of colorectal cancer (CRC); however, the roles of miR‑590‑5p in CRC are not completely understood. Therefore, the present study investigated the expression of miR‑590‑5p and programmed cell death 4 (PDCD4) in CRC tissues and healthy adjacent tissues via reverse transcription‑quantitative PCR. Furthermore, human CRC cells were cultured in vitro and transfected with miR‑590‑5p inhibitor. CRC cell viability, migration and invasion were evaluated by conducting MTT, wound healing and Transwell assays, respectively. Additionally, the relative expression of PDCD4 and phosphorylated‑Smad2/3 was analyzed via western blotting. miR‑590‑5p was significantly upregulated and PDCD4 was significantly downregulated in CRC tissues compared with healthy adjacent tissues. Moreover, the results indicated that miR‑590‑5p knockdown inhibited cell viability and migration by altering the expression of PDCD4, transforming growth factor‑β and phosphorylated‑Smad2/3. PDCD4 was identified as a direct target of miR‑590‑5p. In conclusion, the results of the present study suggested that miR‑590‑5p may regulate CRC cell viability and migration, indicating that miR‑590‑5p may serve as a potential therapeutic target for CRC.