ZENG GUOXIANG1, WANG CHENG2#, TIAN MI3, HE LILI2, WANG MEI2, LI XIN2*
1Department of General Surgery, The People’s Hospital of Hanchuan City, Hanchuan, Hubei, 431600, China - 2Department of General Surgery, The Second People’s Hospital of Jingmen Hubei Province, China - 3Forensic identification institute, Jingmen Public Security Bureau, Hubei, China
Introduction: To study the effect of lentivirus-induced mucin16 (MUC16) gene on cell invasion and metastasis in gallblad- der carcinoma, and the molecular mechanisms involved.
Methods: Gallbladder cell-Shandong (GBC-SD) of over-expression MUC16 and empty viral plasmid-transfected cells were produced through slow virus transfection system. The effect of MUC16 on proliferation of GBC-SC cells in vitro was determined using 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Scratch test and Transwell chambers were used to measure the effect of MUC16 over-expression on in vitro cell migration and invasion. The effect of MUC16 over- expression on GBC-SD cell adhesion was determined with adhesion test, while real time-polymerase chain reaction (RT-PCR) was used to ascertain the pathway involved in MUC16-induced regulation of GBC-SD cell biology.
Results: The growth rate of MUC16 over-expression cells was significantly higher than that of the control group (p <0.05). MUC16 over-expression increased the migration, scratch recovery, and extracellular matrix (ECM) adhesion abilities of GBC-SD cells in vitro. MUC16 significantly enhanced the expression of matrix metalloproteinase-2 (MMP2) and MMP7 mRNAs, relative to control (p < 0.05).
Conclusion: MUC16 enhances the proliferation, invasion and migration of gallbladder carcinoma cells in vitro by activating the PI3K/Akt signal pathway.
Mucoprotein, Gallbladder carcinoma, Proliferation, Invasion, PI3K/Akt signal pathway.