IDDF2019-ABS-0128 Functional mechanism of vascular endothelial growth factor in promoting the growth of intrahepatic cholangiocarcinoma. (June 2019)

• Record Type: Journal Article
• Authors: Wang, Yifei; Liang, Ruiming; Wei, Guangyan; Chu, Hongpeng
• Is Part Of: Gut. Volume 68(2019)Supplement 1
• Page Start: A52
• Page End: A53
• Publication Date: 2019-06
• Subjects: Gastroenterology -- Periodicals; 616.33
• DOI: 10.1136/gutjnl-2019-IDDFAbstracts.93
• Languages: English
• ISSNs: 0017-5749

Abstract

Abstract : Background: To investigate the role of vascular endothelial growth factor (VEGF) and VEGF receptors (VEGFRs) on cell growth of intrahepatic cholangiocarcinoma (ICC). Methods: Western blotting was performed to detect the expression of VEGF in tumour tissues and paired normal tissues from twelve patients with ICC. ICC cell line Huh28 was treated with exogenous recombinant human VEGF (rhVEGF). Cell growth was evaluated by cell counting, proliferation was detected by BrdU cell proliferation assay, and apoptosis was detected by flow cytometry. The expression of VEGF receptors VEGFR1/VEGFR2 in Huh28 cells after rhVEGF treatment was detected by Western blotting. VEGFR1 and VEGFR2 were blocked by specific antibodies, and cell apoptosis was examined by apoptosis-ELISA assay. The stably knockdown VEGFR2 cell line Huh28-shVEGFR2 (experimental group) and the control cell line Huh28-shNC (control group) were established using shRNA lentivirus. Subcutaneous tumour models in ten nude mice with Huh28-shVEGFR2 and Huh28-shNC were used to observe tumour growth. Results: The protein expression of VEGF was up-regulated in ICC tumour tissues than in matched normal tissues ( P <0.01) (figure 1 A). Exogenous rhVEFG could promote the growth of Huh28 cells, suppressed cell apoptosis, without significant effect on cell proliferation ability (figure 1 B-D). The expression of phosphorylated VEGFR1 and VEGFR2 in Huh28 cells were up-regulated after rhVEGF treatment ( P <0.05) (figure 1 E). VEGFR2 antibody could significantly reverse the anti-apoptosis effect of rhVEGF ( P <0.05), while VEGFR1 antibody did not (figure 1 F). Subcutaneous tumour models indicated that tumour growth in the experimental group (Huh28-shVEGFR2) was significantly inhibited compared with the control group (Huh28-shNC) (figure 1 G). Conclusions: VEGF promotes ICC cells growth through inhibiting apoptosis of ICC cells in a VEGFR2-dependent signalling pathway.