International Journal of Medical Sciences · 2022 · 16 citations · 45 references
Life SciencesOncologyPharmacologyApoptosisCancer PharmacologyMolecular OncologyApoptosis In CancerApoptosis ModulationApoptosis RegulationApoptotic SignalingBcl-2 Family ProteinsCaspase ActivationB-cell Lymphoma 2 InhibitionBcl-2 Protein ExpressionBcl-2 Protein RegulationCancer Cell Line ModelsMitochondrial Membrane Potential CollapseMitogen-activated Protein Kinase CascadesMitogen-activated Protein Kinase KinaseMitogen-activated Protein Kinase Pathways
), were investigated in the human bladder cancer cell line 5637. [6]-GIN inhibited cell proliferation, increased sub‑G1 phase ratios, and depolarized mitochondrial membrane potential. [6]-GIN-induced cell death was associated with the downregulation of B‑cell lymphoma 2 (BCL‑2) and survivin and the upregulation of Bcl‑2‑associated X protein (Bax). [6]-GIN activated caspase‑3 and caspase-9 and regulated the activation of mitogen-activated protein kinases (MAPKs). Further, [6]-GIN also increased the intracellular reactive oxygen species (ROS) levels and TG100-115 or tranilast increased [6]-GIN‑induced cell death. These results suggest that [6]-GIN induced apoptosis in the bladder cancer cell line 5637 and therefore has the potential to be used in the development of new drugs for bladder cancer treatment.
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