Genistein Inhibits Cell Growth by Modulating Various Mitogen‐Activated Protein Kinases and AKT in Cervical Cancer Cells

@article{Kim2009GenisteinIC,
  title={Genistein Inhibits Cell Growth by Modulating Various Mitogen‐Activated Protein Kinases and AKT in Cervical Cancer Cells},
  author={Su-Hyeon Kim and Su-Hyeong Kim and Yong‐Beom Kim and Yong Tark Jeon and Sang-C. Lee and Yong Sang Song},
  journal={Annals of the New York Academy of Sciences},
  year={2009},
  volume={1171}
}
Genistein, a soy‐derived isoflavone, inhibits growth of tumor cells from various malignancies. Here we investigated the effect of genistein on the growth of cervical cancer cells (HeLa and CaSki) and its possible mechanism. Genistein significantly suppressed cell growth of HeLa and CaSki cells at concentrations of 20 and 60 μmol/L, respectively, for 24 h. Western blotting analysis showed that genistein reduced phosphorylation of AKT and extracellular signal–regulated kinase (ERK)‐1/2 and… 
Effect of genistein on p90RSK phosphorylation and cell proliferation in T47D breast cancer cells.
TLDR
Concentration-dependent actions of genistein in T47D cells may be due to differential activation of signaling molecules.
Genistein inhibits the proliferation, migration and invasion of the squamous cell carcinoma cells via inhibition of MEK/ERK and JNK signalling pathways.
TLDR
Genistein has a significant anticancer activity in SK-MEL-28 human SCC cells, inducing apoptosis, DNA damage, cell migration and invasion and inhibiting MEK/ERK and JNK signalling pathway.
Effect of Genistein on p 90 RSK Phosphorylation and Cell Proliferation in T 47 D Breast Cancer Cells
TLDR
This study aimed to examine estrogen-receptor (ER)related signaling molecules involved in genistein-associated cell proliferation and survival (ERK1/2, p90RSK, JNK, Akt and NFκB) and to correlate these results to cell proliferation.
Study of Antimetastatic Effect of Genistein Through Inhibition of Expression of Matrix Metalloproteinase in A-549 Cell Line
TLDR
It seems that genistein can decrease recurrence and decreased the migration and invasion of human non-small cell lung cancer cells (A549 cell line) by an efficient antimetastatic effect.
Inhibition of cancer cell invasion and metastasis by genistein
TLDR
The variety of mechanisms by which genistein regulates individual steps of the metastatic cascade are discussed and the potential of this natural product as a promising therapeutic inhibitor of metastasis is highlighted.
Genistein promotes cell death of ethanol-stressed HeLa cells through the continuation of apoptosis or secondary necrosis
TLDR
These results suggested two possible mechanisms through which genistein promoted cell death in stressed cancer cells: Genistein could maintain the existing apoptotic signal to enhance apoptotic cell death and disrupt the recovering process in caspase-independent manner.
Chrysin inhibits cell invasion by inhibition of Recepteur d'origine Nantais via suppressing early growth response-1 and NF-κB transcription factor activities in gastric cancer cells.
TLDR
The results suggest that chrysin has anticancer effects at least by suppressing RON expression through blocking Egr-1 and NF-κB in gastric cancer AGS cells.
Genistein Increase Intracellular Distribution of the High Motility Group Box-1 through p38 Pathway in HeLa culture cells induced by Tumor Necrosis Factor-α
TLDR
There were a strong linkage between p38 activation and HMGB1 translocation in this study, as increasing doses of genistein increase intranuclear p38activation andHMGB1 extranuclear translocation.
...
...

References

SHOWING 1-10 OF 29 REFERENCES
Genistein activates p38 mitogen-activated protein kinase, inactivates ERK1/ERK2 and decreases Cdc25C expression in immortalized human mammary epithelial cells.
TLDR
An important interplay between the p38 pathway and G2 cell cycle checkpoint control is suggested and insights into possible mechanisms whereby this isoflavone may inhibit early events in mammary carcinogenesis are provided.
Inhibition of Nuclear Factor κB Activation in PC3 Cells by Genistein Is Mediated via Akt Signaling Pathway
TLDR
The inhibition of Akt and NF-kappaB activity and their cross-talk provide a novel mechanism by which genistein inhibits cell growth and induces apoptotic processes in tumorigenic but not in nontumorigenic prostate epithelial cells.
Genistein and biochanin A inhibit the growth of human prostate cancer cells but not epidermal growth factor receptor tyrosine autophosphorylation
TLDR
The effect of the isoflavones, genistein, daidzein, and biochanin A on the growth of the LNCaP and DU‐145 human prostate cancer cell lines has been examined, and the mechanism of action does not depend on inhibition of EGF receptors tyrosine autophosphorylation, but on a more distal event in the EGF receptor‐mediated signal transduction cascade.
Taxol-induced apoptosis depends on MAP kinase pathways (ERK and p38) and is independent of p53
TLDR
Data show that both ERK and p38 MAP kinase cascades are essential for apoptotic response to Taxol-induced cellular killing and are independent of p53 activity, however, p53 may serve as a survival factor in breast carcinoma cells treated with Taxol by blocking cells in G2/M phase of the cell cycle.
Inhibitory effect of genistein and daidzein on ovarian cancer cell growth.
TLDR
An inhibitory effect of genistein is demonstrated on ovarian cancer cell growth and colony size by determining caspase-3 activity.
Akt, MAPK (Erk1/2), and p38 Act in Concert to Promote Apoptosis in Response to ErbB Receptor Family Inhibition*
The ErbB receptor family is implicated in the malignant transformation of several tumor types and is overexpressed frequently in breast, ovarian, and other tumors. The mechanism by which CI-1033 and
Prevention of Metastatic Pancreatic Cancer Growth in vivo by Induction of Apoptosis with Genistein, a Naturally Occurring Isoflavonoid
TLDR
Findings suggest that the antimetastatic effect of genistein treatment in vivo is mediated by induction of apoptosis, and may have a therapeutic benefit for patients with pancreatic cancer, in particular after surgery, to prevent recurrence of metastatic disease.
Celecoxib induces apoptosis in cervical cancer cells independent of cyclooxygenase using NF-κB as a possible target
TLDR
Data show that caspase-8 and -9 are involved in the apoptotic effect of celecoxib in cervical cancer cells, which requires the FADD-dependent pathway in a cell type-specific manner and NF-κB may play a key role in Celecoxib-induced apoptosis.
Phosphorylation of Par-4 by Protein Kinase A Is Critical for Apoptosis
TLDR
Evidence is presented that the proapoptotic protein Par-4 utilizes one such common tumorigenic trait to become selectively activated and induce apoptosis in cancer cells, and observations suggest that selective apoptosis of cancer cells by the SAC domain of Par- 4 involves phosphorylation of T155 by PKA.
...
...