Overexpression of HepaCAM Combined with Glutamine Deprivation Inhibits the Proliferation of Prostate Cancer Cells

HE Zhenting¹, LI Ting¹, FAN Jiaxin¹, YUAN Hongling¹, ZHENG Yongbo², WU Xiaohou², LUO Chunli*

(¹Key Laboratory of Diagnostics Medicine of Ministry of Education, Chongqing Medical University, Chongqing 400016, China; ²Department of Urology Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China)

Abstract:

The purpose of this study was to investigate the effect of HepaCAM (hepatecyte cell adhesion molecule) combined with Gln (glutamine) deprivation on glutamine metabolism and proliferation of PCa (prostate cancer) cells. Prostate cancer cell lines PC3 and LNCaP were infected with Ad-HepaCAM adenovirus. Clone formation experiment and MTT assay were used to detect the clonogenesis rate and proliferation activity. The expression of GLS (glutaminase), SLC1A5 (solute carrier family I member V), MYC oncogene family, cyclin D1 and PCNA (proliferating cell nuclear antigen) were detected by qRT-PCR and Western blot. The results showed that overexpression of HepaCAM and deprivation of Gln could inhibit the proliferation of PC3 and LNCaP cells, and the combination of them worked better. qRT-PCR and Western blot showed that compared with the +Gln group (control group), the expression of GLS, SLC1A5 and MYC in the -Gln group (glutamine deprivation group) was up-regulated in a stress-resistant manner, and above the genes were inhibited again after overexpression of Hepa-CAM. This experiment proves that the combination of overexpression of HepaCAM and Gln deprivation can significantly inhibit the proliferation of prostate cancer, and overexpression of HepaCAM can inhibit the reprogramming of glutamine metabolism in prostate cancer cells to some extent.