Publication: Goniothalamin induces mitochondria-mediated apoptosis associated with endoplasmic reticulum stress-induced activation of JNK in HeLa cells
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Issued Date
2017
Resource Type
File Type
application/pdf
ISSN
17921074
Other identifier(s)
2-s2.0-85003874459
Rights Holder(s)
Scopus
Bibliographic Citation
Oncology Letters. Vol 13, No.1 (2017), p.119-128
Suggested Citation
Sophonnithiprasert T., Mahabusarakam W., Nakamura Y., Watanapokasin R. Goniothalamin induces mitochondria-mediated apoptosis associated with endoplasmic reticulum stress-induced activation of JNK in HeLa cells. Oncology Letters. Vol 13, No.1 (2017), p.119-128. doi:10.3892/ol.2016.5381 Retrieved from: https://hdl.handle.net/20.500.14740/4830
Abstract
Goniothalamin, a natural occurring styryl-lactone isolated from Goniothalamus macrophyllus (Blume) Hook. f. & Thomson var. macrophyllus, can trigger cancer cell death in various types of cancer cell. The present study focused on elucidation of the mitochondria-mediated apoptosis associated with endoplasmic reticulum (ER) stress-induced activation of c-Jun NH2-terminal kinase (JNK) by goniothalamin in HeLa cervical cancer cells. Cell viability was determined using an MTT assay, and DNA condensation and loss of mitochondrial membrane potential were determined using Hoechst 33342 and JC-1 staining, respectively. Flow cytometry was used for cell cycle and phosphatidyl-serine exposure analyses. Apoptotic-associated ER stress signaling pathways were determined using immunoblotting, reverse transcription-polymerase chain reaction (RT-PCR) and RT-quantitative PCR analyses. The results suggested that goniothalamin suppressed cell proliferation in a time-and dose-dependent manner. The induction of apoptosis was confirmed by increased DNA condensation, loss of mitochondrial membrane potential and cell surface phosphatidyl-serine presentation. The cell cycle analysis demonstrated that the goniothalamin-treated HeLa cells were in G2/M arrest. Determination of the caspase cascade and apoptotic proteins indicated the induction of apoptosis through the intrinsic pathway. In addition, the levels of phosphorylated JNK and the transcription factor, C/EBP homologous protein (CHOP), an ER stress-associated apoptotic molecule, were increased in the goniothalamin-treated cells. These data indicated that goniothalamin exerted a cytotoxic effect against HeLa cells via the induction of mitochondria-mediated apoptosis, associated with ER stress-induced activation of JNK. © 2017, Spandidos Publications. All rights reserved.
Subject(s)
Glucose regulated protein 78
Mitogen activated protein kinase 1
Mitogen activated protein kinase 3
Protein bcl 2
Protein p53
Stress activated protein kinase
Apoptosis
Article
Cell cycle parameters
Cell proliferation
Controlled study
Cytotoxicity
Disorders of mitochondrial functions
Endoplasmic reticulum stress
Flow cytometry
HeLa cell line
Human
Human cell
IC50
Mitochondrial membrane potential
MTT assay
Polyacrylamide gel electrophoresis
Reverse transcription polymerase chain reaction
Signal transduction
Spectrophotometry
Mitogen activated protein kinase 1
Mitogen activated protein kinase 3
Protein bcl 2
Protein p53
Stress activated protein kinase
Apoptosis
Article
Cell cycle parameters
Cell proliferation
Controlled study
Cytotoxicity
Disorders of mitochondrial functions
Endoplasmic reticulum stress
Flow cytometry
HeLa cell line
Human
Human cell
IC50
Mitochondrial membrane potential
MTT assay
Polyacrylamide gel electrophoresis
Reverse transcription polymerase chain reaction
Signal transduction
Spectrophotometry