Acta Anatomica Sinica ›› 2019, Vol. 50 ›› Issue (5): 613-619.doi: 10.16098/j.issn.0529-1356.2019.05.012

• Cancer Biology • Previous Articles     Next Articles

Mucin 16 regulating activity and migration of gallbladder cancer cells through phosphoinositide 3-kinase/protein kinase B pathway

LI Xin1 TIAN Mi2 PENG Bing1 HE Li-li 3*   

  1. 1.General Surgery of Jingmen Second People’s Hospital, Hubei Jingmen 448000, China; 2.Forensic Medicine of Jingmen Public Security Bureau, Hubei Jingmen 448001, China; 3.Department of Thyroid and Breast Surgery, Jingmen Second People’s Hospital, Hubei Jingmen 448000, China
  • Received:2018-09-06 Revised:2018-12-03 Online:2019-10-06 Published:2019-12-10
  • Contact: HE Li-li E-mail:lilingliling1@qq.com

Abstract:

Objective To investigate the effect of mucin 16(MUC16) on the viability and migration of gallbladder cancer cells (GBC-SD) through phospho inositide 3-kinase/protein kinase B (PI3k/Akt) pathway.   Methods Firstly, after overexpression of MUC16, the matrix metalloproteinase(MMP) family proteins were screened by Real-time PCR. Secondly, after overexpression of MUC16, knockdown of MUC16 and PI3K/Akt pathway inhibitor BKM120, the protein levels of PI3K/Akt pathway and MMP-9 were detected by Western blotting. Finally, the proliferation, viability and migration of gallbladder cancer cells were detected by cell counting kit-8 (CCK-8) and scratch test.  Results After overexpression of MUC16, the relative expression of mRNA in MMP-9 increased significantly (P<0.05). After overexpression of MUC16, the levels of MMP-9, p-Akt and PI3K increased significantly (P<0.05), but PI3K inhibitor BKM120 could avoid this phenomenon. After knocking down MUC16, the protein levels of MMP-9, p-Akt and PI3K decreased  significantly (P<0.05).After overexpression of MUC16, the cell viability and migration ability of GBC-SD increased significantly (P<0.05), while after knocking down MUC16, the cell viability and migration ability of GBC-SD decreased significantly (P<0.05). In addition, after knocking down MMP-9, the cell viability and migration ability of GBC-SD also decreased significantly (P<0.05). However, when MUC16 was overexpressed and MMP-9 was knocked down, there was no significant difference in cell viability and migration ability between GBC-SD and the control group (P>0.05).   Conclusion MUC16 activates PI3K/Akt pathway to promote the expression of MMP-9 protein, thereby enhancing the cell viability and migration of GBC-SD.

Key words: Mucin 16, Phoshoinositide 3-kinase/protein kinase B pathway, Matrix metalloproteinase-9, Gallbladder cancer cell, Western blotting, Real-time PCR, Human