Anti-ADPGK monoclonal antibody

Emerging evidences exposed that long noncoding RNAs (lncRNAs) play important roles in various tumor progression including breast cancer (BC). However, the role of lncRNA ADP-dependent glucokinase antisense RNA 1 (ADPGK-AS1) in BC progression remains undiscovered. Hence, this study aimed to investigate the role of ADPGK-AS1 in BC. qRT-PCR was performed to investigate ADPGK-AS1 expression level in BC tissues and cell lines. The effect of ADPGK-AS1 knockdown on BC cellular process was assessed by loss-of-function assay. Luciferase reporter and RIP assay were performed to investigate the combination between ADPGK-AS1 and miR-3196. The combination between miR-3196 and orthodenticle homeobox 1 (OTX1) was verified by luciferase reporter assay. Finally, rescue assays were performed to confirm the effects of ADPGK-AS1/miR-3196/OTX1 axis on BC development. ADPGK-AS1 expression level was upregulated in BC tissues and cell lines. High expression of ADPGK-AS1 predicted poor prognosis for BC patients. Functionally, ADPGK-AS1 promoted cell proliferation, migration, induced epithelial-mesenchymal transition (EMT) process, and suppressed cell apoptosis. Mechanistically, ADPGK-AS1 acted as a miR-3196 sponge to release OTX1 in BC cells. Currently, ADPGK-AS1 acted as a competing endogenous RNA (ceRNA) via modulating miR-3196/OTX1 axis in BC.

Objective: To verify that high expression of LNCRNA ADPGK-AS1 can increase the sensitivity of gastric cancer (GC) to chemotherapy. Methods: The expression of ADPGK-AS1 in MKN-45, MKN-28, MGC-803, AZ521 and HFE-145 cell lines was detected by qRT-PCR. In addition, si-LncRNA ADPGK-AS1, sh-LncRNA ADPGK-AS1 and Si-NC sequences were transfected into MKN-45 and AZ521 cells. QRT-PCR was employed to detect the ADPGK-AS1 expression in si-LncRNA ADPGK-AS1 and sh-LncRNA groups. MTT, Transwell and flow cytometry (FC) were adopted to test the proliferation, invasion and apoptosis of transfected cells, while Western blot (WB) was utilized to examine the expression of Bax and Bcl-2 in MKN-45 and AZ521 cells. What's more, the cells were respectively subjected to cisplatin (4, 8, 16 and 32 mu mol/L) treatment at different concentrations, and the cell survival was measured 24 hours later. Results: The ADPGK-AS1 level in HFE-145 was significantly higher than that in MKN-45, MKN-28, MGC803 and AZ521 (P<0.05). After transfection, the ADPGK-AS1 level in the MKN-45 and AZ521 cells in the Si-RNA group was significantly lower than that in the Sh-RNA and Si-NC groups (P<0.05). Compared with the Sh-RNA group, the proliferation of MKN-45 and AZ521 in the Si-RNA group was remarkably higher (P<0.05), the invasion capacity was evidently higher (P<0.05) and the apoptosis rate was lower (P<0.05). The Bax protein was reduced statistically in MKN-45 and AZ521 cells in the Si-RNA group (P<0.05), while Bcl-2 protein was increased significantly (P<0.05). At the concentration of 16 mu mol/L and 32 mu mol/L, the survival rate of cells in the Si-RNA group was dramatically higher than that in the other two groups (P<0.05). Conclusion: Highly expressed LncRNA ADPGK-AS1 can inhibit the proliferation and invasion of GC cells and promote apoptosis, and can increase the sensitivity of GC to chemotherapy.