Goniothalamin induces cell cycle-specific apoptosis by modulating the redox status in MDA-MB-231 cells.

  title={Goniothalamin induces cell cycle-specific apoptosis by modulating the redox status in MDA-MB-231 cells.},
  author={Wen-Ying Chen and Chin‐Chung Wu and Yu Hsuan Lan and Fang‐Rong Chang and Che M. Teng and Yang chang Wu},
  journal={European journal of pharmacology},
  volume={522 1-3},
Apoptosis Induction via ATM Phosphorylation, Cell Cycle Arrest, and ER Stress by Goniothalamin and Chemodrugs Combined Effects on Breast Cancer-Derived MDA-MB-231 Cells
Goniothalamin-induced MDA-MB-231 cell apoptosis occurred via intrinsic and extrinsic pathways, along with ER stress, which provide new targeted drug strategies for advancements in anticancer medicine.
Antiproliferative activity of goniothalamin enantiomers involves DNA damage, cell cycle arrest and apoptosis induction in MCF-7 and HB4a cells.
Goniothalamin induces apoptosis associated with autophagy activation through MAPK signaling in SK-BR-3 cells.
Goniothalamin promoted apoptosis associated with autophagy induction in SK-BR-3 cells through p-p38 and p-JNK1/2 upregulation andp-Akt downregulation, indicating that goniothalam may be further used as a potential therapeutic candidate or may offer an alternative treatment for breast cancer.
Goniothalamin Induces Necroptosis and Anoikis in Human Invasive Breast Cancer MDA-MB-231 Cells
An investigation of the anti-cancer activity of GTN and the molecular signaling pathways of non-apoptotic cell death in the invasive human breast cancer MDA-MB-231 cell line were undertaken to determine whether GTN induced cell death and the mechanisms involved.
Goniothalamin induces mitochondria-mediated apoptosis associated with endoplasmic reticulum stress-induced activation of JNK in HeLa cells
The results suggested that goniothalamin suppressed cell proliferation in a time- and dose-dependent manner via the induction of mitochondria-mediated apoptosis, associated with ER stress-induced activation of JNK in HeLa cervical cancer cells.
Apoptosis induction, cell cycle arrest and in vitro anticancer activity of gonothalamin in a cancer cell lines.
It could be concluded that goniothalamin showing a promising cytotoxicity effect against several cancer cell lines including cervical cancer cells (HeLa) with apoptosis as the mode of cell death induced on HeLa cells by Goni hypothalamin was.
(S)-Goniothalamin induces DNA damage, apoptosis, and decrease in BIRC5 messenger RNA levels in NCI-H460 cells
A significant reduction in the messenger RNA levels of baculoviral inhibitor of apoptosis repeat-containing 5 (BIRC5) gene that encodes the survivin protein was found, which may explain the inhibition of cell proliferation and induction of apoptotic induction in tumor cells caused by this compound.
Induction of caspase-9, biochemical assessment and morphological changes caused by apoptosis in cancer cells treated with goniothalamin extracted from Goniothalamus macrophyllus.
It could be concluded that goniothalamin show a promising cytotoxicity effect against cervical cancer cells (Hela) and the cell death mode induced by goni hypothalamin was apoptosis.


Rhein induces apoptosis in HL-60 cells via reactive oxygen species-independent mitochondrial death pathway.
Role of reactive oxygen species and MAPKs in vanadate-induced G(2)/M phase arrest.
Redox-sensitive mechanisms of phytochemical-mediated inhibition of cancer cell proliferation (review).
  • G. Loo
  • Biology, Chemistry
    The Journal of nutritional biochemistry
  • 2003
Induction of apoptosis in breast cancer cells MDA-MB-231 by genistein
Genistein inhibits the growth of MDA-MB-231 breast cancer cells, regulates the expression of apoptosis-related genes, and induces apoptosis through a p53-independent pathway is concluded.
Redox control of cell death.
Mitochondria-specific thioredoxin (Trx-2) and Trx peroxidases (peroxiredoxins) are suggested to regulate cytochrome c release from mitochondria, which is a critical early step in the apoptotis-signaling pathway.
Requirement of Caspase-3(-like) Protease-mediated Hydrogen Peroxide Production for Apoptosis Induced by Various Anticancer Drugs*
Activation of caspase-3(-like) proteases by various anticancer drugs causes generation of H2O2 presumably through the activation of NADPH oxidase, thereby inducing apoptosis, and H1O2 may function as a common mediator for apoptosis induced by various anti-cancer drugs.
Cellular thiols and reactive oxygen species in drug-induced apoptosis.
Recent contributions to the understanding of the importance of cytotoxic drug-induced modulation of cellular redox status for signaling and transcription leading to activation of apoptotic effector mechanisms are summarized.
Cytotoxicity and electron microscopy of cell death induced by goniothalamin.
The cytotoxicity of goniothalamin was found to be strong towards both cancerous (HGC-27, MCF-7, PANC-1, HeLa), and non-cancerous (3T3) cell lines, especially in cases of dividing cells. Drug exposure