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| Naturally occurring element. Selenium is incorporated into selenoproteins, such as glutathione peroxidases (GPxs) and thioredoxin reductases (TrxRs), which play critical roles in protecting cells from oxidative damage. Involved in GPx, TrxR, ans Selenoprotien P which protect normal cells from oxidative stress. Important in Thyroid hormone metabolism, immune system regulation, reproductive health, and Brain and heart protection. -recommended daily allowance (RDA) for selenium is about 55 µg/day for adults. (upper tolerance 400ug/day) -One Brazil nut may contain 50-300ug/nut Sodium selenite (Na₂SeO₃) is a selenium compound with well-documented anticancer and chemopreventive properties -Oxidation state: +4 (selenite form of selenium) -Type: Inorganic selenium compound (water-soluble) -Sodium selenite generates reactive oxygen species (ROS) selectively in tumor cells. -Induces cytochrome c release, caspase-3 activation, and DNA fragmentation. -Reduces VEGF expression and endothelial cell migration. -Blocks cell division at G2/M phase -Suppresses MMP-2 and MMP-9 activity -Activates p53 -Inhibits NF-κB -PI3K/Akt/mTOR Suppression -Inactivation of Thioredoxin/Glutathione systems -NRF2 inhibition in cancer cell might be connected with O2 level Narrow therapeutic window: -Low micromolar (≤5 µM) → anticancer -High (>10 µM) → toxic to normal cells Some Selenium Supplements use Sodium Selenite as the active ingredient. - NOW Foods Selenium, Nature's Bounty Selenium, etc Other common form is Selenomethionine, as it is better absorbed (found in brazil nuts), but might be less effective? | Category | Role in cancer | | -------------------------------- | ----------------------------------------------------------------------------------------------- | | Sodium Selenium (selenite) | Direct cytotoxic redox poison | | Selenium (organic / nutritional) | **Redox buffer & immune modulator** (generally *anti-therapy* when oxidative stress is desired) | | SeNPs | Tunable redox-signaling anticancer platform | Selenium (Organic / Nutritional) — Cancer-Relevant Pathways
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| Also known as CP32. Cysteinyl aspartate specific proteinase-3 (Caspase-3) is a common key protein in the apoptosis and pyroptosis pathways, and when activated, the expression level of tumor suppressor gene Gasdermin E (GSDME) determines the mechanism of tumor cell death. As a key protein of apoptosis, caspase-3 can also cleave GSDME and induce pyroptosis. Loss of caspase activity is an important cause of tumor progression. Many anticancer strategies rely on the promotion of apoptosis in cancer cells as a means to shrink tumors. Crucial for apoptotic function are executioner caspases, most notably caspase-3, that proteolyze a variety of proteins, inducing cell death. Paradoxically, overexpression of procaspase-3 (PC-3), the low-activity zymogen precursor to caspase-3, has been reported in a variety of cancer types. Until recently, this counterintuitive overexpression of a pro-apoptotic protein in cancer has been puzzling. Recent studies suggest subapoptotic caspase-3 activity may promote oncogenic transformation, a possible explanation for the enigmatic overexpression of PC-3. Herein, the overexpression of PC-3 in cancer and its mechanistic basis is reviewed; collectively, the data suggest the potential for exploitation of PC-3 overexpression with PC-3 activators as a targeted anticancer strategy. Caspase 3 is the main effector caspase and has a key role in apoptosis. In many types of cancer, including breast, lung, and colon cancer, caspase-3 expression is reduced or absent. On the other hand, some studies have shown that high levels of caspase-3 expression can be associated with a better prognosis in certain types of cancer, such as breast cancer. This suggests that caspase-3 may play a role in the elimination of cancer cells, and that therapies aimed at activating caspase-3 may be effective in treating certain types of cancer. Procaspase-3 is a apoptotic marker protein. Prognostic significance: • High Cas3 expression: Associated with good prognosis and increased sensitivity to chemotherapy in breast, gastric, lung, and pancreatic cancers. • Low Cas3 expression: Linked to poor prognosis and increased risk of recurrence in colorectal, hepatocellular carcinoma, ovarian, and prostate cancers. |
| 4484- | Se, | Chit, | PEG, | Anti-cancer potential of selenium-chitosan-polyethylene glycol-carvacrol nanocomposites in multiple myeloma U266 cells |
| - | in-vitro, | Melanoma, | U266 |
| 4486- | Se, | Chit, | Selenium-Modified Chitosan Induces HepG2 Cell Apoptosis and Differential Protein Analysis |
| - | in-vitro, | Liver, | HepG2 |
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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