08/02/2025
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Yes
New XGEF growth factor has been found which stimulates Gq releasing IP3 & DAG , & thus intracellular calcium is released enhancing breast cancer. Yes other factors on seven trans membranes domain Gi & Gs act differently. Gi is inhibitory & Gs upregulates (adenyl Cyclase ) & thus cAMP decrease or increase. Even up regulation of cGMP, no calcium release . It is only by stimulation of Gq ( G coupled receptors on seven transmemberane domain receptors by XGEF only which spreads breast cancer.
When a new growth factor like XGEF binds to a seven transmembrane domain receptor on the surface of endothelial cells, it triggers a signaling cascade that leads to increased intracellular calcium levels, potentially promoting angiogenesis (new blood vessel formation) which is critical for cancer cell growth and metastasis; this occurs through activation of phospholipase C (PLC), which then hydrolyzes phosphatidylinositol 4,5-bisphosphate (PIP2) into inositol 1,4,5-trisphosphate (IP3) that subsequently releases calcium from the endoplasmic reticulum stores within the cell. [1, 2, 3]
Key points about this mechanism: [1, 2]
• Receptor activation: XGEF binding to its seven transmembrane domain receptor on the endothelial cell initiates a signaling cascade by activating G proteins coupled to the receptor.
• Phospholipase C (PLC) activation: Activated G proteins stimulate PLC enzyme, which then cleaves PIP2 into IP3 and diacylglycerol (DAG).
• Calcium release from ER: IP3 binds to receptors on the endoplasmic reticulum (ER), causing the release of stored calcium ions into the cytoplasm, leading to a rise in intracellular calcium concentration. [1, 2]
How this contributes to cancer development: [2, 4]
• Angiogenesis: Increased calcium levels in endothelial cells can stimulate the expression of pro-angiogenic factors like vascular endothelial growth factor (VEGF), promoting the formation of new blood vessels which supply oxygen and nutrients to rapidly growing tumor cells. [2, 4]
• Cell migration and invasion: Calcium signaling plays a crucial role in cell motility and adhesion, which are critical for cancer cell migration and invasion into surrounding tissues. [1, 2, 5]
• Tumor microenvironment: By influencing the behavior of endothelial cells, XGEF can modify the tumor microenvironment, creating favorable conditions for cancer cell growth and metastasis. [2, 3, 5]
Important considerations: [2, 3, 6]
• Specificity of XGEF: Further research is needed to determine the specific signaling pathway downstream of XGEF and its unique role compared to other growth factors involved in angiogenesis.
• Therapeutic potential: Understanding the XGEF-mediated calcium signaling pathway could lead to the development of targeted therapies to inhibit angiogenesis and cancer progression by blocking XGEF activity or its downstream signaling components. [2, 3, 6]
Generative AI is experimental.
[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC7074364/[2] https://pubmed.ncbi.nlm.nih.gov/16301830/[3] https://my.clevelandclinic.org/health/articles/24206-angiogenesis[4] https://en.wikipedia.org/wiki/Vascular_endothelial_growth_factor[5] https://www.sciencedirect.com/science/article/pii/S1044579X15000231[6] https://pmc.ncbi.nlm.nih.gov/articles/PMC3756375/
Yes , now can we find a drug to counter breast carcinoma by counteracting this new XGEF
HER2
