Aspernolide A Inhibits the Proliferation of Human Laryngeal Carcinoma Cells through the Mitochondrial Apoptotic and STAT3 Signaling Pathways.

Abstract

Aspernolide A, a butyrolactone secondary metabolite, was purified from the endophytic fungus Cladosporium cladosporioides derived from roots of Camptotheca acuminata Decne. In this study, the antitumor activity and mechanisms of aspernolide A on human laryngeal cancer Hep-2 and TU212 cells were studied by MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay, morphological observation and Western blotting. The results showed that aspernolide A significantly inhibited the proliferation of Hep-2 and TU212 cells in dose- and time-dependent manners. Morphological changes of apoptotic cells could be observed under an inverted microscope, such as irregular margins, decreased adherence ability and chromatin condensation. The expressions of Bax, Caspase-9, Caspase-3 and PARP (poly ADP-ribose polymerase) increased with the increase of dosage while Bcl-2 decreased, suggesting that the apoptotic mechanism might be related to the mitochondrial apoptotic pathway. Moreover, the expression of the phosphorylation of STAT3 decreased with the increase of dosage, suggesting that the apoptotic mechanism might be related to the STAT3 signaling pathway. All these conclusions indicated that aspernolide A has the potential anti-laryngocarcinoma effects.

• Authors: Chang Liu, Hong Liu, Yanzhang Wen, Huiqi Huang, Ji Hao, Yibing Lv, Rui Qin, Xinzhou Yang
• Journal: Molecules (Basel, Switzerland) (Molecules) Vol. 24 Issue 6 (Mar 19 2019) ISSN: 1420-3049 [Electronic] Switzerland
• PMID: 30893785 (Publication Type: Journal Article)

Chemical References

• STAT3 Transcription Factor
• aspernolide A
• bcl-2-Associated X Protein
• CASP3 protein, human
• Caspase 3
• Caspase 9
• 4-Butyrolactone

Topics

• 4-Butyrolactone (analogs & derivatives, pharmacology)
• Apoptosis (drug effects)
• Caspase 3 (metabolism)
• Caspase 9 (metabolism)
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Humans
• Laryngeal Neoplasms (metabolism)
• Membrane Potential, Mitochondrial (drug effects)
• Mitochondria (drug effects, metabolism)
• STAT3 Transcription Factor (metabolism)
• Signal Transduction (drug effects)
• bcl-2-Associated X Protein (metabolism)