Mitochondrial fission promotes cell migration by Ca2+/CaMKII/ERK/FAK pathway in hepatocellular carcinoma

• DOI: 10.1111/liv.13660
• Publication Date: 2017-12-06T06:26:39Z
• Authors: Xiacheng Sun; Haiyan Cao; Lei Zhan; Chun Yin; Gang Wang; Ping Liang; Jibin Li; Zhe Wang; Bingrong Liu; Qichao Huang; Jinliang Xing
• Keywords: DNM1L; MFN2

Abstract Background & Aims Mitochondrial dynamics of fission and fusion plays critical roles in a diverse range important cellular functions, its deregulation has been increasingly implicated human diseases. Previous studies have shown that increased mitochondrial significantly promoted the proliferation hepatocellular carcinoma (HCC) cells. However, how they influence migration tumour cells remained largely unknown. Methods In present study, we further investigated effect on metastasis Moreover, underlying molecular mechanisms therapeutic application were explored. Results Our data showed dynamin‐1‐like protein expression was strongly distant when compared to primary carcinoma. contrast, mitofusin 1 an opposite trend. associated with disease‐free survival patients. addition, our reprogramming focal‐adhesion lamellipodia formation mainly by activating typical Ca 2+ /CaMKII/ERK/FAK pathway. Importantly, treatment division inhibitor‐1 decreased calcium signalling had potential for vivo. Conclusions Taken together, findings demonstrate role regulation cell migration, which provides strong evidence this process as drug target treatment.