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| Isobavachalcone - Prenylated Chalcone Type: Natural prenylated chalcone / flavonoid-related phytochemical Sources: Found in several medicinal plants, particularly Psoralea corylifolia (Cullen corylifolium), as well as other plant species containing prenylated chalcones. Function: Isobavachalcone is a bioactive prenylated chalcone with anticancer, anti-inflammatory, antioxidant, antimicrobial, and neuroprotective activities. Reported molecular effects include modulation of AKT, ERK/MAPK, ROS, apoptosis, inflammatory signaling, and cellular stress pathways. Cancer: Experimental studies demonstrate inhibition of cancer-cell proliferation, migration, and invasion and induction of apoptosis and other forms of regulated cell death. IBC can suppress AKT and ERK signaling, increase tumor-cell oxidative stress, and modulate antitumor immune responses. Anticancer activity has been demonstrated in pancreatic, breast, oral, colorectal, thyroid, and other experimental cancer models. Alzheimer's Disease: Preclinical studies indicate neuroprotective activity, including reduction of Aβ accumulation and plaque pathology, suppression of neuroinflammation, and improvement of memory and cognitive deficits in Alzheimer's disease models. |
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| In all eukaryotic cells, intracellular Ca2+ levels are maintained at low resting concentrations (approximately 100 nM) by the activity of the major Ca2+ extrusion system, the plasma membrane Ca2+-ATPase (PMCA), which exchanges extracellular protons (H+) for cytosolic Ca2+. Indeed, sustained elevation of [Ca2+]C in the form of overload, saturating all Ca2+-dependent effectors, prolonged decrease in [Ca2+]ER, causing ER stress response, and high [Ca2+]M, inducing mitochondrial permeability transition (MPT), are considered to be pro-death factors. In cancer the Ca2+-handling toolkit undergoes profound remodelling (figure 1) to favour activation of Ca2+-dependent transcription factors, such as the nuclear factor of activated T cells (NFAT), c-Myc, c-Jun, c-Fos that promote hypertrophic growth via induction of the expression of the G1 and G1/S phase transition cyclins (D and E) and associated cyclin-dependent kinases (CDK4 and CDK2). Thus, cancer cells may evade apoptosis through decreasing calcium influx into the cytoplasm. This can be achieved by either downregulation of the expression of plasma membrane Ca2+-permeable ion channels or by reducing the effectiveness of the signalling pathways that activate these channels. Such protective measures would largely diminish the possibility of Ca2+ overload in response to pro-apoptotic stimuli, thereby impairing the effectiveness of mitochondrial and cytoplasmic apoptotic pathways. Voltage-Gated Calcium Channels (VGCCs): Overexpression of VGCCs has been associated with increased tumor growth and metastasis in various cancers, including breast and prostate cancer. Store-Operated Calcium Entry (SOCE): SOCE mechanisms, such as STIM1 and ORAI1, are often upregulated in cancer cells, contributing to enhanced cell survival and proliferation. High intracellular calcium levels are associated with increased cell proliferation and migration, leading to a poorer prognosis. Calcium signaling can also influence hormone receptor status, affecting treatment responses. Increased Ca²⁺ signaling is associated with advanced disease and metastasis. Patients with higher CaSR expression may have a worse prognosis due to enhanced tumor growth and resistance to apoptosis. -Ca2+ is an important regulator of the electric charge distribution of bio-membranes. |
| 7385- | IBC, | Fighting cancer by triggering non-canonical mitochondrial permeability transition-driven necrosis through reactive oxygen species induction |
| - | vitro+vivo, | Lung, | A549 | - | in-vitro, | BC, | 4T1 |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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