|
KMID : 0620920180500100130
|
|
Experimental & Molecular Medicine
2018 Volume.50 No. 10 p.130 ~ p.130
|
|
|
CLOCK and BMAL1 stabilize and activate RHOA to promote F-actin formation in cancer cells
|
|
Ma Teng-Jiao
Zhang Zhi-Wei
Lu Yi-Lu
Zhang Ying-Ying
Tao Da-Chang
Liu Yun-Qiang
Ma Yong-Xin
|
|
|
Abstract
|
|
|
|
Circadian genes control most of the physiological functions in cancer cells, including cell proliferation, migration, and invasion. The CLOCK and BMAL1 complex plays a central role in circadian rhythms. Previous studies have shown that circadian genes may act as oncogenes or tumor-suppressor genes. In addition, F-actin, regulated by RHOA, has been shown to participate in tumor progression. However, the roles of the CLOCK and BMAL1 genes in the regulation of tumor progression via the RHOA-ROCK-CFL pathway remain largely unclear. Here we first indicate that the rearrangement of F-actin is regulated by CLOCK and BMAL1. We found that CLOCK and BMAL1 can upregulate RHOA expression by inhibiting CUL3-mediated ubiquitination and activate RHOA by reducing the interaction between RHOA and RhoGDI. Consequently, CLOCK and BMAL1 control the expression of the components of the RHOA-ROCK-CFL pathway, which alters the dynamics of F-actin/G-actin turnover and promotes cancer cell proliferation, migration, and invasion. In conclusion, our research proposes a novel insight into the role of CLOCK and BMAL1 in tumor cells.
|
|
|
KEYWORD
|
|
|
Cancer of unknown primary, RHO signalling
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
    
|
|