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[6]-Gingerol induces Caspase-Dependent Apoptosis in Bladder Cancer cells via MAPK and ROS Signaling

The anti-cancer effects of [6]-gingerol ([6]-GIN), the main active polyphenol of ginger (Zingiber officinale), 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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The study you mentioned investigated the anti-cancer effects of [6]-gingerol ([6]-GIN), which is the main active polyphenol found in ginger (Zingiber officinale), specifically in the human bladder cancer cell line 5637. The researchers found that [6]-GIN had several effects on the cancer cells.

Firstly, [6]-GIN inhibited the proliferation of the bladder cancer cells, meaning it prevented their rapid and uncontrolled growth. This is a desirable effect as uncontrolled cell growth is a hallmark of cancer.

Furthermore, [6]-GIN increased the sub-G1 phase ratios in the cancer cells. The sub-G1 phase is a part of the cell cycle associated with cell death (apoptosis). An increase in the sub-G1 phase suggests that [6]-GIN induced apoptosis in the bladder cancer cells.

The researchers also observed that [6]-GIN caused depolarization of the mitochondrial membrane potential. Mitochondria play a crucial role in cell survival and energy production. Disruption of the mitochondrial membrane potential is often associated with cell death.

In addition, [6]-GIN downregulated the expression of B-cell lymphoma 2 (BCL-2) and survivin, which are proteins involved in promoting cell survival and inhibiting apoptosis. Conversely, [6]-GIN upregulated the expression of Bcl-2-associated X protein (Bax), which promotes apoptosis.

The study also demonstrated that [6]-GIN activated caspase-3 and caspase-9, which are enzymes involved in the apoptotic process. Caspases play a key role in the execution of apoptosis by breaking down various cellular components.

Furthermore, [6]-GIN affected the activation of mitogen-activated protein kinases (MAPKs). MAPKs are a family of proteins involved in cell signaling pathways that regulate various cellular processes, including cell growth, differentiation, and apoptosis.

Moreover, [6]-GIN increased the levels of reactive oxygen species (ROS) within the cancer cells. ROS are highly reactive molecules that can cause oxidative damage to cells. Increased ROS levels can induce cell death in cancer cells.

Importantly, the researchers found that the combination of [6]-GIN with TG100-115 or tranilast, which are other compounds, further enhanced the cell death induced by [6]-GIN. This suggests a potential synergistic effect when [6]-GIN is combined with other drugs or compounds.

Based on these findings, the study suggests that [6]-GIN has the potential to induce apoptosis in bladder cancer cells and could be considered for the development of new drugs for bladder cancer treatment. However, further research is necessary to validate these findings and determine the potential clinical application of [6]-GIN in bladder cancer therapy.

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S1352 TG100-115 TG100-115 is a PI3Kγ/δ inhibitor with IC50 of 83 nM/235 nM, with little effect on PI3Kα/β. Phase 1/2.

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PI3K