Fig. 4

Apoptosis induction in cancer cells by gossypol. Gossypol interferes with cellular function by causing mitochondrial dysfunction, which leads to an increase in reactive oxygen species (ROS). This accumulation of ROS results in oxidative stress that damages cellular components, including DNA. Concurrently, gossypol's interaction with mitochondria leads to ATP depletion, crippling the cell’s energy supply and further exacerbating cellular stress. The compound also hinders key survival signals by downregulating Akt, a protein essential for cell survival, and c-Myc, a transcription factor that supports cell growth and proliferation. Additionally, gossypol inhibits the activity of telomerase reverse transcriptase (TERT), an enzyme vital for maintaining telomere length and thereby cell longevity. Together, these actions culminate in the activation of the cell’s apoptotic pathways, leading to programmed cell death. ↑ increase, ↓ decrease, telomerase reverse transcriptase (TERT), Adenosine triphosphate (ATP), Cellular myelocytomatosis oncogene (c-MyC), serine/threonine protein kinase (Akt)