Long non-coding RNA CACNA1G-AS1 promotes calcium channel protein expression and positively affects human keloid fibroblast migration

• Published in: Oncology letters Vol. 16; no. 1; pp. 891 - 897
• Main Authors: Li, Ye, Liang, Xuebing, Wang, Peng, Long, Xiao, Wang, Xiaojun, Meng, Zhiqiang
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications 01.07.2018; Spandidos Publications UK Ltd; D.A. Spandidos
• Subjects: Apoptosis; Bladder cancer; Cancer therapies; Care and treatment; Cell adhesion & migration; Cell cycle; Cell growth; Collagen; Development and progression; Extracellular matrix; Fibroblasts; Gene expression; Genetic aspects; Growth factors; Health aspects; Hyperplasia; Keloids; Melanoma; Oncology; Protein expression; Proteins; RNA; Studies; Surgery; Beijing China; United States > US; China; calcium channel; keloid; long noncoding RNA; fibroblast; CACNA1G-AS1
• ISSN: 1792-1074; 1792-1082
• DOI: 10.3892/ol.2018.8717

Keloids are a type of benign hyperplasia that cause dermatologic dysfunction and esthetic deformity by invading adjacent normal tissues. Little is known about their etiology, therefore, they are a challenge to treat using plastic surgery. In a previous study, it was demonstrated that the expression of the long non-coding RNA CACNA1G-AS1 (CAS1) is high in keloid tissue, suggesting that CAS1 is involved in keloid formation. In the present study, the aim was to identify potential keloid target proteins by exploring CAS1 biological function during cell proliferation and migration, cytokine secretion, collagen secretion and the control of calcium channel protein expression in human keloid fibroblasts. Three biopsy samples were collected from each patient with keloids at The Peking Union Medical College Hospital, which were then used to investigate the role of CAS1 in cell proliferation and migration. CAS1 silencing was also carried out using small interfering RNA; cell factors, collagen and calcium channel protein levels were compared with control cells. The interference of CAS1 expression reached 50% compared with the control group. CACNA1G and type I collagen expression was significantly downregulated by CAS1 knockdown, while the expression of transforming growth factor-β and type III collagen was not affected. Wound healing time was longer in the CAS1-knockdown group, but there was no visible change in cell proliferation. In conclusion, CAS1 appeared to promote calcium channel protein and type I collagen expression, and to have a positive effect on cell migration in human keloid fibroblasts. Therefore it has potential as a novel therapeutic target for keloids.