Exploring a Novel Role of Glycerol Kinase 1 in Prostate Cancer PC-3 Cells.
Bobae ParkSang-Hun KimSun-Nyoung YuKwang-Youn KimHoyeon JeonSoon-Cheol AhnPublished in: Biomolecules (2024)
Clinically, prostate cancer is infamous for its histological and molecular heterogeneity, which causes great challenges to pinpoint therapy and pharmaceutical development. To overcome these difficulties, researchers are focusing on modulating tumor microenvironment and immune responses in addition to genetic alteration and epigenetic regulation. Here, we aimed to identify potential biomarkers or modulators of prostate cancer by investigating genes specifically altered in prostate cancer cells treated with established anti-cancer agents. Glycerol kinase 1 (GK1) is phosphotransferase encoded on the X chromosome, is associated with the synthesis of triglycerides and glycerophospholipids, and has been mainly studied for X-linked metabolic disorder GK deficiency (GKD). Interestingly, our DNA microarray analysis showed that several anti-cancer agents highly induced the expression of GK1, especially GK1a and GK1b isoforms, in human prostate cancer PC-3 cells. To elucidate the relationship between GK1 and cancer cell death, a human GK1b-specific expression vector was constructed and transfected into the PC-3 cells. Surprisingly, GK1b overexpression dramatically reduced cell viability and significantly accelerated apoptotic cell death. These findings suggest that GK1b may serve as a promising modulator and biomarker of cell death in prostate cancer, offering potential avenues for therapeutic intervention.
Keyphrases
- prostate cancer
- cell death
- radical prostatectomy
- endothelial cells
- immune response
- poor prognosis
- randomized controlled trial
- cell cycle arrest
- genome wide
- copy number
- single cell
- stem cells
- cell proliferation
- transcription factor
- squamous cell carcinoma
- induced pluripotent stem cells
- papillary thyroid
- bone marrow
- inflammatory response
- high glucose
- oxidative stress
- dendritic cells
- young adults
- cell free
- dna methylation
- toll like receptor
- replacement therapy