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| Type: |
| Protein expression of ATF, GRP78, and GADD153 which is a hall marker of ER stress. The endoplasmic reticulum (ER) stress signaling pathway plays a crucial role in maintaining cellular homeostasis and responding to various stressors, including those encountered in cancer. When cells experience stress, such as the accumulation of misfolded proteins, they activate a series of signaling pathways collectively known as the unfolded protein response (UPR). The UPR aims to restore normal function by enhancing the protein-folding capacity of the ER, degrading misfolded proteins, and, if the stress is unresolved, triggering apoptosis. The activation of ER stress pathways can contribute to resistance against chemotherapy and targeted therapies. Cancer cells may utilize the UPR to survive treatment-induced stress, making it challenging to achieve effective therapeutic outcomes. -ER stress-associated proteins include: phosphorylation of PERK, eIF2α, ATF4, CHOP and cleaved-caspase 12 |
| Glioblastoma is a fast-growing and aggressive brain tumor. |
| 5272- | 3BP, | The efficacy of the anticancer 3-bromopyruvate is potentiated by antimycin and menadione by unbalancing mitochondrial ROS production and disposal in U118 glioblastoma cells |
| - | in-vitro, | GBM, | U87MG | - | in-vitro, | Nor, | HEK293 |
| 4563- | AgNPs, | Rad, | Silver nanoparticles enhance neutron radiation sensitivity in cancer cells: An in vitro study |
| - | in-vitro, | BC, | MCF-7 | - | in-vitro, | Ovarian, | SKOV3 | - | in-vitro, | GBM, | U87MG | - | in-vitro, | Melanoma, | A431 |
| 3345- | ART/DHA, | Dihydroartemisinin-induced unfolded protein response feedback attenuates ferroptosis via PERK/ATF4/HSPA5 pathway in glioma cells |
| - | in-vitro, | GBM, | NA |
| 5133- | ART/DHA, | Dihydroartemisinin Exerts Anti-Tumor Activity by Inducing Mitochondrion and Endoplasmic Reticulum Apoptosis and Autophagic Cell Death in Human Glioblastoma Cells |
| - | in-vitro, | GBM, | U87MG | - | in-vitro, | GBM, | U251 |
| 1402- | BBR, | Berberine-induced apoptosis in human glioblastoma T98G cells is mediated by endoplasmic reticulum stress accompanying reactive oxygen species and mitochondrial dysfunction |
| - | in-vitro, | GBM, | T98G |
| 5674- | BTZ, | Bortezomib-induced unfolded protein response increases oncolytic HSV-1 replication resulting in synergistic, anti-tumor effects |
| - | in-vivo, | GBM, | NA | - | in-vivo, | HNSCC, | NA |
| 2903- | LT, | Luteolin induces apoptosis by ROS/ER stress and mitochondrial dysfunction in gliomablastoma |
| - | in-vitro, | GBM, | U251 | - | in-vitro, | GBM, | U87MG | - | in-vivo, | NA, | NA |
| 3458- | MF, | Magnetic Control of Protein Expression via Magneto-mechanical Actuation of ND-PEGylated Iron Oxide Nanocubes for Cell Therapy |
| - | in-vitro, | GBM, | NA |
| 2065- | PB, | TMZ, | Inhibition of Mitochondria- and Endoplasmic Reticulum Stress-Mediated Autophagy Augments Temozolomide-Induced Apoptosis in Glioma Cells |
| - | in-vitro, | GBM, | NA |
| 1943- | PL, | Piperlongumine treatment inactivates peroxiredoxin 4, exacerbates endoplasmic reticulum stress, and preferentially kills high-grade glioma cells |
| - | in-vitro, | GBM, | NA | - | in-vivo, | NA, | NA |
| 5125- | Sal, | Salinomycin induced ROS results in abortive autophagy and leads to regulated necrosis in glioblastoma |
| - | in-vitro, | GBM, | NA |
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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:27 Cells:% prod#:% Target#:103 State#:% Dir#:2
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