Shangfeng Sun1, Weiwei Li2, Xiaomin Ma2, Hong Luan3. 1. Department of Colorectal Anal Surgery, The Central Hospital of Zaozhuang Mining Group of Shandong, Qilianshan Road, High-Tech Zone, Zaozhuang, China. 2. Department of Clinical Laboratory, The Central Hospital of Zaozhuang Mining Group of Shandong, Qilianshan Road, High-Tech Zone, Zaozhuang, China. 3. Department of Colorectal Anal Surgery, The Central Hospital of Zaozhuang Mining Group of Shandong, Qilianshan Road, High-Tech Zone, Zaozhuang, China, luanhong8686@163.com.
Abstract
AIM: To examine the expression status of long-noncoding RNA LINC00265 and mechanistically elucidate its involvements in colorectal cancer (CRC). METHODS: Relative abundances of LINC00265, miR-216b-5p, and tripartite-motif (TRIM)44 transcript were determined with real-time polymerase chain reaction. Cell viability was measured with cell counting kit-8 kit. Glucose uptake, pyruvate, and lactate production were quantified with commercially available kits. The potential regulatory effects of miR-216b-5p on both LINC00265 and TRIM44 were interrogated by luciferase reporter assay. The direct association between miR-216b-5p with both LINC00265 and TRIM44 was analyzed with pull-down assay. The TRIM44 protein was quantitated by western blotting. RESULTS: LINC00265 was upregulated in CRC both in vivo and in vitro, which intimately associated with poorer prognosis. LINC00265-deficiency resulted into decreases in cell viability, glucose uptake, pyruvate production, and lactate production. Mechanistically, LINC00265 directly bound to miR-216b-5p and negatively regulated miR-216b-5p. Consequently, the suppression on TRIM44 expression was released. Supplementation with ectopic miR-216b-5p significantly compromised the oncogenic activities of LINC00265 in CRC cells. CONCLUSION: Our study highlighted the contribution of LINC00265/miR-216b-5p/TRIM44 signaling axis in CRC.
AIM: To examine the expression status of long-noncoding RNA LINC00265 and mechanistically elucidate its involvements in colorectal cancer (CRC). METHODS: Relative abundances of LINC00265, miR-216b-5p, and tripartite-motif (TRIM)44 transcript were determined with real-time polymerase chain reaction. Cell viability was measured with cell counting kit-8 kit. Glucose uptake, pyruvate, and lactate production were quantified with commercially available kits. The potential regulatory effects of miR-216b-5p on both LINC00265 and TRIM44 were interrogated by luciferase reporter assay. The direct association between miR-216b-5p with both LINC00265 and TRIM44 was analyzed with pull-down assay. The TRIM44 protein was quantitated by western blotting. RESULTS:LINC00265 was upregulated in CRC both in vivo and in vitro, which intimately associated with poorer prognosis. LINC00265-deficiency resulted into decreases in cell viability, glucose uptake, pyruvate production, and lactate production. Mechanistically, LINC00265 directly bound to miR-216b-5p and negatively regulated miR-216b-5p. Consequently, the suppression on TRIM44 expression was released. Supplementation with ectopic miR-216b-5p significantly compromised the oncogenic activities of LINC00265 in CRC cells. CONCLUSION: Our study highlighted the contribution of LINC00265/miR-216b-5p/TRIM44 signaling axis in CRC.