| Literature DB >> 33196934 |
Kun Fan1,2,3,4, Dexiang Zhang1, Min Li2,3,4, Sheng Shen2,3,4, Jiwen Wang2,3,4, Xiaojian Ni2,3,4, Zijun Gong2,3,4, Bohao Zheng2,3,4, Zhihui Gao2,3,4, Xiaoling Ni2,3,4, Tao Suo5,6,7, Han Liu8,9,10, Houbao Liu11,12,13,14.
Abstract
CA-125, coded by MUC16 gene, is responsible to many kinds of tumor metastasis. However, the related mechanism remains unclear. We have established a novel manner to reveal gallbladder cancer metastasis related to serum CA-125 levels through the C-terminal polypeptide of MUC16 gene production. MUC16 C-terminal polypeptide significantly promoted gallbladder cancer cell migration and invasion in vitro. Mass spectrum indicated that interaction of MUC16 C-terminal fragment with the C-terminal domain of stathmin1 inhibited the phosphorylation of stathmin1 to promote the combination with tubulin. Stathmin1 knockdown inhibited the migration and invasion of gallbladder cancer cells in vitro and lung metastasis in vivo induced by MUC16 C-terminal polypeptide. The high expression level of MUC16c consistent with stathmin1 was also confirmed in gallbladder cancer tissues. Our study revealed the underlying mechanism of gallbladder cancer metastasis related to CA-125 levels, which was beneficial for CA-125 in gallbladder cancer diagnose and therapy.Entities:
Keywords: Gallbladder cancer; MUC16 C-terminal; Metastasis; Microtubule; Stathmin1
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Year: 2020 PMID： 33196934 DOI： 10.1007/s12032-020-01438-x
Source DB: PubMed Journal: Med Oncol ISSN： 1357-0560 Impact factor: 3.064