STUDIES ON THE MOLECULAR MECHANISMS INVOLVED IN SLOW VIRUS-INDUCED MUC16 GENE EFFECT ON CELL INVASION AND METASTASIS IN GALLBLADDER CARCINOMA

ZENG GUOXIANG¹, WANG CHENG^2#, TIAN MI³, HE LILI², WANG MEI², LI XIN^2*

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.