Nano-hydroxyapatite promotes cell apoptosis by co-activating endoplasmic reticulum stress and mitochondria damage to inhibit glioma growth
Contact us if these videos are not relevant.
Contact us if these videos are not relevant.
View abstract on PubMed
Summary
This summary is machine-generated.Nano-hydroxyapatite (n-HA) triggers cancer cell death by inducing endoplasmic reticulum (ER) stress and mitochondrial damage. This study clarifies n-HA
Area Of Science
- Biomaterials Science
- Cancer Biology
- Cellular and Molecular Mechanisms
Background
- Nano-hydroxyapatite (n-HA) shows anti-tumor effects, but its precise mechanisms are not fully understood.
- Endoplasmic reticulum (ER) and mitochondria are crucial for calcium (Ca2+) homeostasis and cellular stress responses.
- The interplay between ER and mitochondria in Ca2+ regulation is vital for preventing cellular damage.
Purpose Of The Study
- To investigate the anti-tumor effectiveness of needle-like n-HA.
- To elucidate the underlying cellular and molecular mechanisms of n-HA's anti-glioma effects.
- To explore the role of ER-mitochondria interplay in n-HA-induced cancer cell apoptosis.
Main Methods
- Fabrication of needle-like nano-hydroxyapatite (n-HA).
- In vitro studies on glioma cell growth and invasion.
- Analysis of ER stress biomarkers, intracellular reactive oxygen species, and mitochondrial membrane potential.
- In vivo experiments to assess tumor growth inhibition.
Main Results
- n-HA significantly reduced glioma cell growth and invasion in vitro.
- n-HA treatment upregulated ER stress biomarkers (GRP78, p-IRE1, p-PERK, PERK, ATF6) and activated CHOP, inducing apoptosis.
- n-HA caused increased reactive oxygen species, mitochondrial membrane depolarization, and downstream apoptotic signaling, indicating Ca2+ overload and mitochondrial damage.
- In vivo studies confirmed n-HA's ability to induce ER stress and mitochondrial damage, effectively restraining glioma tumor growth.
Conclusions
- n-HA induces cancer cell apoptosis by co-activating ER stress and mitochondrial damage.
- The findings offer new insights into ER-mitochondria targeted anti-tumor therapies.
- n-HA presents a promising therapeutic agent for glioma treatment.
Contact us if these videos are not relevant.
Contact us if these videos are not relevant.
Related Concept Videos
Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or immature dendritic cells. Non-professional phagocytes such as epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes.
Normal cells contain receptors that prevent them from being recognized...
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...