Diosgenin induces cell cycle arrest and apoptosis in human leukemia K562 cells with the disruption of Ca2+ homeostasis

  title={Diosgenin induces cell cycle arrest and apoptosis in human leukemia K562 cells with the disruption of Ca2+ homeostasis},
  author={Ming-Jie Liu and Zhao Wang and Yong Ju and Ricky Ngok-shun Wong and Qing-yu Wu},
  journal={Cancer Chemotherapy and Pharmacology},
PurposeDiosgenin is a steroidal sapogenin with estrogenic and antitumor properties. In order to elucidate the mechanism of its antiproliferative activity, we investigated its effects on the cell cycle and apoptosis in human chronic myelogenous leukemia K562 cells.MethodsCell viability was assessed via an MTT assay. Apoptosis was investigated in terms of nuclear morphology, DNA fragmentation, and phosphatidylserine externalization. Cell cycle analysis was performed via PI staining and flow… 

Induction of G2/M Phase Arrest by Diosgenin via Activation of Chk1 Kinase and Cdc25C Regulatory Pathways to Promote Apoptosis in Human Breast Cancer Cells

Findings reveal that the anti-proliferative activity of diosgenin involves the induction of G2/M phase arrest via modulating the Cdc25C-Cdc2-cyclin B pathway and mitochondria-mediated apoptosis in human breast cancer cell lines, which suggests the potential usefulness of diOSgenin in treating breast cancer.

Salidroside induces apoptosis via ERK 1 / 2 in human leukemia K 562 cells

It is suggested that salidroside inhibits cell viability and induces cell cycle arrest and apoptosis via inactivation of ERK1/2 signaling pathway in human leukemia K562 cells and may be a promising candidate for leukemia treatment.

Diosgenin increases BBC3 expression in HepG2/C3A cells and alters cell communication in a 3D spheroid model


Diosgenin may serve as a potential candidate in the prevention of cell proliferation and enhances apoptosis in oral cancer cells Hep-2 and KB.

Diosgenin Induces Apoptosis in HepG2 Cells through Generation of Reactive Oxygen Species and Mitochondrial Pathway

Results suggest that diosgenin-induced apoptosis in HepG2 cells through Bcl-2 protein family-mediated mitochndria/caspase-3-dependent pathway and this oxidative stress might induce apoptosis through activation of ASK1, which are critical upstream signals for JNK/p38 MAPK activation in hepatitisG2 cancer cells.

Yamogenin-Induced Cell Cycle Arrest, Oxidative Stress, and Apoptosis in Human Ovarian Cancer Cell Line

This work shows that yamogenin induces apoptosis in ovarian cancer cells, and both the extrinsic and mitochondrial—intrinsic pathways are involved in this process.

Diosgenin induces ROS-dependent autophagy and cytotoxicity via mTOR signaling pathway in chronic myeloid leukemia cells.

Puerarin attenuates the daunorubicin-induced apoptosis of H9c2 cells by activating the PI3K/Akt signaling pathway via the inhibition of Ca2+ influx.

Puerarin attenuates the DNR-induced apoptosis of H9c2 cells by activating the PI3K/Akt signaling pathway via the inhibition of Ca2+ influx, suggesting that puerarin may be a potential cardioprotective agent for use in the clinical treatment of cardiomyopathy triggered by DNR.



Different contribution of apoptosis to the antiproliferative effects of diosgenin and other plant steroids, hecogenin and tigogenin, on human 1547 osteosarcoma cells.

It was showed that diosgenin strongly enhanced the activation of p53 in contrast to hecogenin and tigogenin actions, and this biological action seems correlated with a large increase of p 53 protein expression.

Modulation of Mitochondrial Ca2+ Homeostasis by Bcl-2*

Evidence is provided that the maintenance of Ca m homeostasis is essential for cell survival, and both ER and mitochondrial Ca2+ stores are important, and the depletion of either one will result in apoptosis.

Tumor Necrosis Factor-induced Apoptosis Stimulates p53 Accumulation and p21WAF1 Proteolysis in ME-180 Cells*

Evidence is provided for the early onset of genotoxic stress in cells committed to TNF-mediated apoptosis and for divergence in propagation of this signal in non-responsive cells.

Cleavage of CDK Inhibitor p21Cip1/Waf1 by Caspases Is an Early Event during DNA Damage-induced Apoptosis*

It is reported here that human p21 protein is rapidly induced but selectively cleaved during the apoptotic response to γ-irradiation, suggesting that p21 may serve as a critical checkpoint regulator for both cell cycle arrest and apoptosis during the p53-mediated DNA damage response.

Caspase-mediated cleavage of p21Waf1/Cip1 converts cancer cells from growth arrest to undergoing apoptosis

The cyclin-dependent kinase inhibitor p21Waf1/Cip1 is a downstream effector of the p53-dependent cell growth arrest. We report herein that p21 was cleaved by caspase-3/CPP32 at the site of DHVD112↓L

p53 regulates mitochondrial membrane potential through reactive oxygen species and induces cytochrome c‐independent apoptosis blocked by Bcl‐2

The ROS‐mediated disruption of Δψ constitutes a pivotal step in the apoptotic pathway of p53, and this pathway does not involve cytochrome c release.

Regulation of the G2/M transition by p53

Evidence that implicates p53 in controlling entry into mitosis when cells enter G2 with damaged DNA or when they are arrested in S phase due to depletion of the substrates required for DNA synthesis is reviewed.

BCL-2 family members and the mitochondria in apoptosis.

As the BCL-2 family members reside upstream of irreversible cellular damage and focus much of their efforts at the level of mitochondria, they play a pivotal role in deciding whether a cell will live or die, and it is argued that the amphipathic a-helical BH3 domain serves as a critical death domain in the pro-apoptotic members.

Changes in intramitochondrial and cytosolic pH: early events that modulate caspase activation during apoptosis

It is shown that mitochondria-mediated alteration of intracellular pH may be an early event that regulates caspase activation in the mitochondrial pathway for apoptosis, and this finding is supported by results obtained from cells using protonophores.