Decreasing Microtubule Actin Cross-Linking Factor 1 Inhibits Melanoma Metastasis by Decreasing Epithelial to Mesenchymal Transition
Received 29 August 2019
Accepted for publication 28 December 2019
Published 29 January 2020 Volume 2020:12 Pages 663—673
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 3
Editor who approved publication: Dr Yong Teng
Xiaoying Wang, 1 Xiao Jian, 1 Jun Dou, 2 Zicheng Wei, 3 Fengshu Zhao 2
1Wuxi School of Medicine, Jiangnan University, Wuxi, People’s Republic of China; 2Department of Pathogenic Biology and Immunology, School of Medicine, Southeast University, Nanjing, People’s Republic of China; 3Department of Stomatology Affiliated Hospital of Jiangnan University, Wuxi, People’s Republic of China
Correspondence: Jun Dou; Fengshu Zhao
Department of Pathogenic Biology and Immunology, Medical School, Southeast University, 87 Dingjiaqiao Road, Nanjing 210009, People’s Republic of China
Email firstname.lastname@example.org; Fengshu_zhao@126.com
Background: The microtubule actin cross-linking factor 1 (MACF1) is involved in cellular migration, adhesion, and invasion processes. Its abnormal expression initiates tumor cell proliferation and metastasis in numerous cancer types.
Methods: In this study, we utilized short hair-pin RNA interference of MACF1 to assess the inhibitory effects on the metastatic potential of B16F10 melanoma cells both in vitro and in vivo a mouse model.
Results: The MACF1 expression was increased in B16F10 cells-induced tumor tissues; while the down-regulation of MACF1 impacted the B16F10 melanoma cell metastatic behavior by decreasing the ability of colony formation and invasion in vitro as well as inhibiting B16F10 cells-induced tumor growth and lung metastasis in vivo. The results of Western blot and immunohistochemistry indicated that the expression of E-cadherin and Smad-7 was significantly increased whereas the expression of N-cadherin and TGF-β 1 was significantly decreased in tumor tissue of mice challenged with the B16F10/MACF1-RNAi cells when compared with the B16F10 cells challenged mice.
Conclusion: The data presented in this study demonstrated that down-regulated MACF1 expression decreased B16F10 melanoma metastasis in mice by inhibiting the epithelial to mesenchymal transition program. Thus, MACF1 may be a novel target for melanoma therapy.
Keywords: melanoma, microtubule actin cross-linking factor 1, metastasis, epithelial to mesenchymal transition
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