fig3

Figure 3. Ca²⁺ signalling pathways in cancer cells. GPCRs mediate cellular pathways such as MAPK, CaMKKβ/AMPKα/mTOR, and PI3K/Akt, thereby exerting regulatory control over Ca²⁺ channels. Consequently, Ca²⁺ ions modulate these cell pathways. The generation and regulation of transcription factors lead to cancer cell proliferation, EMT, metastasis, invasion, and survival. Akt and Murine Double Minute 2 (MDM2) inhibit Bad and p53, respectively, thereby supporting evasion from apoptosis. Inhibition of p53 releases Bcl-2, which in turn inhibits apoptosis. STAT3 and NFκB promote EMT, while mTOR promotes cell proliferation and cytoprotective autophagy. Transcription factors such as c-Fos, c-Jun, c-Myc, and CREB play pivotal roles in gene transcription crucial for cellular growth. VGCC: voltage-gated Ca²⁺ channel; SOCE: store-operated Ca²⁺ entry; TRP: transient receptor potential; GPCR: G-protein coupled receptor; PLC: phospholipase C; PIP2: phosphatidylinositol 4,5-bisphosphate; DAG: diacylglycerol; IP3: inositol-1,4,5-trisphosphate; PKC: protein kinase C; RAS: rat sarcoma; RAF: rapidly accelerated fibrosarcoma; ERK: extracellular signal-regulated kinase; JNK: c-Jun N-terminal kinase; STAT3: signal transducer and activator of transcription 3; MAPK: mitogen-activated protein kinases; NFκB: nuclear factor-κB; CREB: cyclic adenosine monophosphate-responsive element-binding; AC: adenylyl cyclase; PKA: protein kinase A; cAMP: cyclic adenosine monophosphate; PI3K: phosphatidylinositol 3-kinase; EMT: epithelial-mesenchymal transition.