Open AccessUnconventional myosin VIIA promotes melanoma progression
Author(s) -
Yuqing Liu,
Xiaofan Wei,
Lina Guan,
Sidi Xu,
Yuan Yang,
Decheng Lv,
Xiao He,
Jun Zhan,
Yan Kong,
Jun Guo,
Hongquan Zhang
Publication year - 2018
Publication title -
journal of cell science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.384
H-Index - 278
eISSN - 1477-9137
pISSN - 0021-9533
DOI - 10.1242/jcs.209924
Subject(s) - biology , melanoma , downregulation and upregulation , cancer research , gene silencing , myosin , microbiology and biotechnology , cell migration , rna interference , cell , genetics , gene , rna
Unconventional myosin VIIA (Myo7a) is an actin-based motor molecule that normally functions in cochlear hair cells of the inner ear. Mutations of MYO7A/Myo7a have been implicated in inherited deafness in both humans and mice. However, there is limited information about the functions of Myo7a outside of the specialized cells of the ears. Herein, we report a previously-unidentified function of Myo7a by demonstrating that it plays an important role in melanoma progression. We found that silencing Myo7a by RNAi inhibited melanoma cell growth by upregulation of cell cycle regulator p21 and suppressed melanoma cell migration and invasion by downregulation of RhoGDI2 and MMP9. Further, Myo7a depletion suppressed melanoma cell metastases to the lung, kidney, and bone in mice. In contrast, overexpression of Myo7a promoted melanoma xenograft growth and lung metastasis. Importantly, Myo7a levels are remarkably elevated in human melanoma patients. Collectively, we demonstrated for the first time that Myo7a is able to function in non-specialized cells, a finding that reveals the complicated disease-related roles of Myo7a, especially in melanomas.