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Anti-glioblastoma Activity of Kaempferol via Programmed Cell Death Induction: Involvement of Autophagy and Pyroptosis.

ABSTRACT: Glioblastoma is one of the most common and lethal intracranial malignant, and is still lack of ideal treatments. Kaempferol is a major nutrient found in various edible plants, which has exhibited the potential for the treatment of glioblastoma. However, the specific anti-glioma mechanism of kaempferol is yet to be studied. Herein, we aim to explore the mechanisms underlying the anti-glioma activity of kaempferol. Our results demonstrated that kaempferol suppresses glioma cell proliferation in vitro and inhibits tumor growth in vivo. Moreover, kaempferol raises ROS and decreases mitochondrial membrane potential in glioma cells. The high levels of ROS induce autophagy then ultimately trigger the pyroptosis of glioma cells. Interestingly, when we used 3-MA to inhibit autophagy, we found that the cleaved form of GSDME was also decreased, suggesting that kaempferol induces pyroptosis through regulating autophagy in glioma cells. In conclusion, this study revealed kaempferol possesses good anti-glioma activity by inducing ROS, and subsequently leads to autophagy and pyroptosis, highlighting its clinical potentials as a natural nutrient against glioblastoma.

SUBMITTER: Chen S

PROVIDER: S-EPMC7758214 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Anti-glioblastoma Activity of Kaempferol via Programmed Cell Death Induction: Involvement of Autophagy and Pyroptosis.

Chen Suqin S Ma Jing J Yang Liu L Teng Muzhou M Lai Zheng-Quan ZQ Chen Xiaoyu X He Jingjin J

Frontiers in bioengineering and biotechnology 20201210

Glioblastoma is one of the most common and lethal intracranial malignant, and is still lack of ideal treatments. Kaempferol is a major nutrient found in various edible plants, which has exhibited the potential for the treatment of glioblastoma. However, the specific anti-glioma mechanism of kaempferol is yet to be studied. Herein, we aim to explore the mechanisms underlying the anti-glioma activity of kaempferol. Our results demonstrated that kaempferol suppresses glioma cell proliferation <i>in ...[more]

PMID: 33363136

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Project description:BackgroundGraves' disease (GD) is associated with thyroid stimulating hormone (TSH) receptor (TSHR) antibodies of variable bioactivity. We have previously characterized "neutral" TSHR antibodies (N-TSHR-Abs) that bind to the hinge region of the TSHR ectodomain. We showed that an N-TSHR monoclonal antibody (mAb) failed to induce any G proteins to sustain survival signaling and lead to excessive stress and apoptosis. Furthermore, the addition of TSH, or the antioxidant N-acetyl-l-cysteine (NAC), rescued N-TSHR-mAb-induced apoptotic death. However, the detailed mechanisms of this rescue remained unclear.MethodsAutophagy is activated in response to diverse stress related stimuli so we have, therefore, studied the autophagy response in rat thyroid cells (FRTL-5) during N-TSHR-mAb induced thyrocyte stress and apoptosis using the In Cell Western technique for quantitation along with immunocytochemistry.ResultsUnder starvation conditions with N-TSHR-mAb the addition of TSH or NAC prevented thyroid cell death by enhancing autophagy. This was evidenced by elevated levels of autophagy related proteins including beclin 1, LC3A, LC3B, ULK1, p62, and also activated pink and perkin mitophagy related proteins. The phenomenon was further confirmed by image analyses using Cyto-ID and Mito-ID autophagy detection systems. We also found that either TSH or NAC enhanced PKA, Akt, mTORC, AMPK, Sirtuins, PGC1α, NRF-2, mitofusin-2, TFAM and catalase in the N-TSHR-mAb stressed cells. Thus TSH or NAC restored cell survival signaling which reduced cell stress and enhanced mitochondrial biogenesis. The N-TSHR-mAb also activated cytochrome-C, Bax, caspase-9, caspase-3A, and had less effect on FADD or caspase-8 indicating activation of the intrinsic pathway for apoptosis.ConclusionsThese findings indicated that TSH or antioxidant can rescue thyroid cells from N-TSHR-mAb induced apoptosis via enhanced autophagy. These observations signify that N-TSHR-mAb in GD under low TSH conditions caused by the hyperthyroidism could be detrimental for thyrocyte survival which would be another factor able to precipitate ongoing autoinflammation.

Dataset Information

Anti-glioblastoma Activity of Kaempferol via Programmed Cell Death Induction: Involvement of Autophagy and Pyroptosis.

Publications

Anti-glioblastoma Activity of Kaempferol via Programmed Cell Death Induction: Involvement of Autophagy and Pyroptosis.

Similar Datasets

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