ReferenceID 4579
Asiatic Acid Induces Endoplasmic Reticulum Stress and Activates the Grp78/IRE1α/JNK and Calpain Pathways to Inhibit Tongue Cancer Growth
Front Pharmacol
Asiatic acid (AA) has been shown to induce apoptotic death in a range of cancers, but the mechanisms whereby it can inhibit tongue cancer growth have yet to be clarified. Herein, we explored the effects of AA on tongue c
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Record Fields
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- Reference Id
- 4579
- Evidence Id
- 21169
- Core Evidence Id
- 21169
- Source Reference Id
- 2431
- Herb2 Reference Id
- HBREF003228
- Subject Paper Key
- HBIN017057_34122116
- Pubmed Id
- 34122116
- Doi
- 10.3389/fphar.2021.690612
- Paper Title
- Asiatic Acid Induces Endoplasmic Reticulum Stress and Activates the Grp78/IRE1α/JNK and Calpain Pathways to Inhibit Tongue Cancer Growth
- Paper Abstract
- Asiatic acid (AA) has been shown to induce apoptotic death in a range of cancers, but the mechanisms whereby it can inhibit tongue cancer growth have yet to be clarified. Herein, we explored the effects of AA on tongue cancer cells and found that it induced their apoptotic death in vitro and in vivo, while additionally impairing xenograft tumor growth in vivo. From a mechanistic perspective, AA treatment was associated with increases in levels of calcium and the calcium- dependent protease calpain, and it further induced endoplasmic reticulum (ER) stress and consequent Grp78-related IRE1alpha and JNK phosphorylation, ultimately driving caspase-3 activation and apoptotic death. Together, these results highlight AA as a promising tool for the therapeutic treatment of tongue cancer in clinical practice.
- Journal
- Front Pharmacol
- Publish Year
- 2021
- Experiment Subject
- Experiment Type
- Cell Experiment
- Phenotype Related
- Cancers; Tumor; Tongue Cancer
- Paper Title Cn
- Paper Title En
- Asiatic Acid Induces Endoplasmic Reticulum Stress and Activates the Grp78/IRE1α/JNK and Calpain Pathways to Inhibit Tongue Cancer Growth
- Bilingual Status
- semi_complete