Abstract
Long non‑coding RNAs (lncRNAs) are involved in colorectal cancer (CRC) progression, however the mechanisms remain largely unknown. The present study aimed to reveal the role and possible molecular mechanisms of a new LNCRNA, LINC00858, in CRC. LINC00858 was increased in CRC tumor tissues, and patients with high LINC00858 expression had a shorter survival time. Knockdown of LINC00858 expression suppressed cell proliferation and induced G0/G1 cell cycle arrest and apoptosis in TP53‑wild‑type CRC cells. Subsequently, using Starbase v2.0 database, miR‑25‑3p was confirmed to interact with LINC00858 and was downregulated by LINC00858. Reduction of miR‑25‑3p expression with an inhibitor significantly attenuated the biological effects of LINC00858 knockdown in CRC cells. Furthermore, using TargetScan, SMAD7 was validated to interact with miR‑25‑3p and was downregulated by miR‑25‑3p. Lastly, the ectopic overexpression of SMAD7 rescued the suppressive effects of LINC00858 knockdown in CRC cells. Collectively, the results from the present study, to the best of our knowledge, firstly demonstrated a novel LINC00858/miR‑25‑3p/SMAD7 regulatory axis that promoted CRC progression, indicating LINC00858 as a promising therapeutic target for CRC.