Abstract
Purpose: To investigate the effects of Krüppel-like factor 8 (KLF8) in prostate cancer (PCa) cell viability and glycolysis, and explore its role as a regulatory factor.Methods: Immunoblot assays were conducted to assess the expression of KLF8 and proteins in AKT/mTOR pathway in PCa cell lines PC-3 and DU145. Cell Counting Kit-8 assays were performed to assess the effect of KLF8 on PCa cell viability. The glycolysis capacity of PCa cells was determined by measuring the levels of glucose intake, lactic acid production, and cellular ATP levels.Results: Depletion of KLF8 decreased the survival of PCa cells in vitro (p < 0.05). KLF8 depletion also inhibited aerobic glucose metabolism in PCa cells (p < 0.05). Further studies confirmed that KLF8 contributed to the growth and glycolysis of PCa cells via the regulation of AKT/mTOR pathway.Conclusion: KLF8 regulates glycolysis in PCa cells by regulating AKT/mTOR signaling pathway and is thus a promising therapeutic target for PCa treatment.
 Keywords: Krüppel-like factor 8 (KLF8), Prostate cancer (PCa), Aerobic glucose, AKT/mTOR signaling pathway, Therapeutic target
Highlights
Prostate cancer (PCa) is a malignant tumor caused by excessive proliferation of prostatic epithelial cells [1]
This study suggests that Krüppel-like factor 8 (KLF8) could serve as a novel therapeutic target for the treatment of PCa
The glycolysis levels of PCa cells were evaluated according to the glucose intake, lactic acid production, and cellular ATP levels, which were measured using the corresponding kits from Abcam Company (Cambridge, UK)
Summary
Prostate cancer (PCa) is a malignant tumor caused by excessive proliferation of prostatic epithelial cells [1]. This study suggests that KLF8 could serve as a novel therapeutic target for the treatment of PCa. The AKT/PI3K inhibitor LY294002 (CAS#: 154447-36-6, R&D Systems, Minneapolis, MN, USA) was administered at a final concentration of 20 μM in PCa cells for 24 hours. For the in vitro experiments, PC-3 and DU145 cells were transfected with p-LKO.1-KLF8 shRNA plasmids to deplete the expression of KLF8. KLF8 depletion significantly inhibited the viability of PC-3 and DU145 cells in vitro (Figure 1B). The glycolysis levels of PCa cells were evaluated according to the glucose intake (ab136955), lactic acid production (ab83429), and cellular ATP levels (ab83355), which were measured using the corresponding kits from Abcam Company (Cambridge, UK). Lactate production levels and cellular ATP levels decreased after the transfection of KLF8 shRNA plasmids in PC-3 and DU145 cells (Figure 2 B and C).
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