Adiponectin inhibits vascular smooth muscle cell calcification induced by beta-glycerophosphate through JAK2/STAT3 signaling pathway

Radioresistance is a material obstacle for effective treatment of colorectal cancer (CRC). Thus, the discovery of a novelbiomarker for determining the CRC radiosensitivity is necessary. Recent studies have confirmed that miR-183-3p regulatescell phenotypes and tumor growth in various cancers. However, the role and mechanism of this micro-ribonucleic acid inCRC radiosensitivity remains unclear. Here, the abundances of miR-183-5p and ATG5 mRNA were detected by a real-timequantitative reverse transcription polymerase chain reaction. Kaplan–Meier survival analysis was carried out to explore thecorrelation between miR-183-5p and patient prognosis. Cell viability was evaluated by the MTT assay. Survival fractionanalysis through colony formation was performed to assess the cell radiation response. Bioinformatic, luciferase andwestern blot assays were employed to verify the targeted interaction between miR-183-5p and ATG5. The results showedthat an elevated abundance of miR-183-5p and a reduced ATG5 level in CRC were associated with the poor prognosis. Theknockdown of miR-183-5p enhanced the sensitivity of CRC cells to radiation, inflected by the decreased cell viability andsurvival fraction. Mechanically, ATG5 was targeted by miR-183-5p. The addition of ATG5 conferred the radiosensitivity ofthe CRC cells, which was revered by miR-183-5p restoration. Furthermore, miR-183-5p knockdown hindered the tumorgrowth by repressing ATG5 in vivo after radiation treatment. In summary, the output data indicated that miR-183-5pheightened the radiation response of the CRC cells by targeting ATG5, promising a novel therapeutic target for CRCpatients with radioresistance.