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| GRP78 (Pgp, BiP or ERp72) is a central regulator of endoplasmic reticulum (ER) function due to its roles in protein folding and assembly, targeting misfolded protein for degradation, ER Ca(2+)-binding and controlling the activation of trans-membrane ER stress sensors. -GRP78 protein, a marker for endoplasmic reticulum stress -GRP78’s role as a master regulator of the unfolded protein response (UPR) and cellular stress responses The association of P-gp and inhibition of cell death in cancerous cells has also been reported in several studies including in hepatocellular, colorectal, prostate cancer, and gastric cancer. Although counterintuitive due to its prominent role in cancer resistance, P-gp has been linked to favorable prognosis. ERp72 can promote cancer cell proliferation, migration, and invasion by regulating various signaling pathways, including the PI3K/AKT and MAPK/ERK pathways. Additionally, ERp72 can also inhibit apoptosis (programmed cell death) in cancer cells, which can contribute to tumor progression. Overexpressed in: Breast, lung colorectal, prostrate, ovarian, pancreatic. -GRP78 is frequently upregulated in a variety of solid tumors and hematological malignancies. -Overexpression of GRP78 in cancer cells is often regarded as a marker of increased ER stress due to the reduced oxygen and nutrient supply typically encountered in the tumor microenvironment. -Elevated GRP78 levels can contribute to tumor cell survival by enhancing the adaptive UPR, allowing cancer cells to cope with therapeutic and metabolic stress. |
| Normal Healthy |
| 4561- | AgNPs, | VitC, | Cellular Effects Nanosilver on Cancer and Non-cancer Cells: Potential Environmental and Human Health Impacts |
| - | in-vitro, | CRC, | HCT116 | - | in-vitro, | Nor, | HEK293 |
| 2732- | BetA, | Chemo, | Betulinic acid chemosensitizes breast cancer by triggering ER stress-mediated apoptosis by directly targeting GRP78 |
| - | in-vitro, | BC, | MCF-7 | - | in-vitro, | BC, | MDA-MB-231 | - | in-vitro, | Nor, | MCF10 |
| 744- | Bor, | Borax affects cellular viability by inducing ER stress in hepatocellular carcinoma cells by targeting SLC12A5 |
| - | in-vitro, | HCC, | HepG2 | - | in-vitro, | Nor, | HL7702 |
| 6010- | CGA, | The Biological Activity Mechanism of Chlorogenic Acid and Its Applications in Food Industry: A Review |
| - | Review, | Nor, | NA |
| 3208- | EGCG, | Induction of Endoplasmic Reticulum Stress Pathway by Green Tea Epigallocatechin-3-Gallate (EGCG) in Colorectal Cancer Cells: Activation of PERK/p-eIF2α/ATF4 and IRE1α |
| - | in-vitro, | Colon, | HT29 | - | in-vitro, | Nor, | 3T3 |
| 2841- | FIS, | Fisetin, an Anti-Inflammatory Agent, Overcomes Radioresistance by Activating the PERK-ATF4-CHOP Axis in Liver Cancer |
| - | in-vitro, | Nor, | RAW264.7 | - | in-vitro, | Liver, | HepG2 | - | in-vitro, | Liver, | Hep3B | - | in-vitro, | Liver, | HUH7 |
| 3416- | TQ, | Thymoquinone induces apoptosis in bladder cancer cell via endoplasmic reticulum stress-dependent mitochondrial pathway |
| - | in-vitro, | Bladder, | T24/HTB-9 | - | in-vitro, | Bladder, | 253J | - | in-vitro, | Nor, | SV-HUC-1 |
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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