Zhiqi Song1, Jingrong Lin2, Zhe Sun1, Jing Ni1, Yang Sha1. 1. Department of Dermatology, The 1st Affiliated Hospital of Dalian Medical University, No. 222, Zhongshan Road, Dalian 116011, China. 2. Department of Dermatology, The 1st Affiliated Hospital of Dalian Medical University, No. 222, Zhongshan Road, Dalian 116011, China. Electronic address: amy4963@163.com.
Abstract
BACKGROUND: Cyclin-dependent kinase-like 1 (CDKL1) is a member of cell division control protein 2 (CDC-2)-related serine threonine protein kinase family, and is reported to be overexpressed in malignant tumors such as breast cancer and gastric cancer. OBJECTIVE: This study aimed to evaluate the whether CDKL1 can serve as a potential molecular target for melanoma gene therapy. METHODS: CDKL1 expression in two melanoma cell lines, A375 and MV3 was measured by real-time PCR. To investigate the role of CDKL1 in cell growth of melanoma, we constructed CDKL1-siRNA expressing lentivirus and infected A375 and MV3 cells. The effects of RNAi-mediated CDKL1 downregulation on A375 and MV3 cell proliferation and colony-formation ability were detected by methylthiazoletetrazolium (MTT) assay and colony-formation assay. The effects of CDKL1 downregulation on A375 and MV3 cell cycle and apoptosis were analyzed by FACS analysis. RESULTS: Human melanoma cell lines A375 and MV3 expressed CDKL1 mRNA. Knockdown of CDKL1 in A375 and MV3 by CDKL1-siRNA lentivirus infection significantly inhibited cell growth and colony formation ability, promoted cell apoptosis, and arrested cells in G1 phase. CONCLUSION: CDKL1 is associated with melanoma cell growth, colony formation, apoptosis, and cell cycle regulation. It may be considered as a valuable target for anti-melanoma therapeutic strategies.
BACKGROUND:Cyclin-dependent kinase-like 1 (CDKL1) is a member of cell division control protein 2 (CDC-2)-related serine threonine protein kinase family, and is reported to be overexpressed in malignant tumors such as breast cancer and gastric cancer. OBJECTIVE: This study aimed to evaluate the whether CDKL1 can serve as a potential molecular target for melanoma gene therapy. METHODS:CDKL1 expression in two melanoma cell lines, A375 and MV3 was measured by real-time PCR. To investigate the role of CDKL1 in cell growth of melanoma, we constructed CDKL1-siRNA expressing lentivirus and infected A375 and MV3 cells. The effects of RNAi-mediated CDKL1 downregulation on A375 and MV3 cell proliferation and colony-formation ability were detected by methylthiazoletetrazolium (MTT) assay and colony-formation assay. The effects of CDKL1 downregulation on A375 and MV3 cell cycle and apoptosis were analyzed by FACS analysis. RESULTS:Humanmelanoma cell lines A375 and MV3 expressed CDKL1 mRNA. Knockdown of CDKL1 in A375 and MV3 by CDKL1-siRNA lentivirus infection significantly inhibited cell growth and colony formation ability, promoted cell apoptosis, and arrested cells in G1 phase. CONCLUSION:CDKL1 is associated with melanoma cell growth, colony formation, apoptosis, and cell cycle regulation. It may be considered as a valuable target for anti-melanoma therapeutic strategies.