Silymarin Inhibits Cervical Cancer Cell Through an Increase of Phosphatase and Tensin Homolog

@article{Yu2012SilymarinIC,
  title={Silymarin Inhibits Cervical Cancer Cell Through an Increase of Phosphatase and Tensin Homolog},
  author={Hann-Chin Yu and Li-Jen Chen and Kai Cheng and Yingxiao Li and Ching Hua Yeh and Juei-Tang Cheng},
  journal={Phytotherapy Research},
  year={2012},
  volume={26}
}
Silymarin is an active constituent contained in the seeds of the milk thistle plant and is widely used as a hepatic protection agent due to its antioxidant‐like activity. In the present study we evaluated the potential action of silymarin against cervical cancer and investigated its mechanism of action. Treatment of cervical cancer cells (C‐33A) with silymarin resulted in a significant decrease in cell viability. Silymarin induced apoptosis through the modulation of Bcl‐2 family proteins and… 
Increase of phosphatase and tensin homolog by silymarin to inhibit human pharynx squamous cancer.
TLDR
The results suggest that silymarin inhibits the Akt signaling pathway by increasing PTEN expression in FaDu cells and directly affects Bcl-2 family members and demonstrates the inhibitory activity of sily marin for oral cancer is related to cell survival.
In vitro and in vivo anti-cancer activity of silymarin on oral cancer
  • Dong-Hoon Won, L. Kim, +8 authors Sung-Dae Cho
  • Biology, Medicine
    Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • 2018
TLDR
In vitro and in vivo evidence is provided supporting the anti-cancer effect of silymarin and death receptor 5, and caspase-8 may be essential players in sily marin-mediated apoptosis in oral cancer.
Silymarin inhibits Toll-like receptor 8 gene expression and apoptosis in Ramos cancer cell line
TLDR
Results indicated a new mechanism in the anticancer activity of Toll-like receptor (TLR) signaling after silymarin treatment in Ramos cancer cell line, which could be used to develop anticancer agents inhibiting TLRs.
Dual Effects of Silymarin on Nasopharyngeal Carcinoma Cells (NPC-TW01)
TLDR
Silymarin at a low dose can induce cytostatic effect on TW01 cells mainly through an increase of antioxidant-like action, and should be applied carefully to patients with nasopharyngeal carcinoma.
Increase in apoptosis by combination of metformin with silibinin in human colorectal cancer cells.
TLDR
The combined treatment of human colorectal cancer cells with silibinin and metformin may induce apoptosis at a dose that does not affect HCoEpiC, revealing a potential therapeutic strategy for the treatment of coloreCTal cancer.
Silymarin antiproliferative and apoptotic effects: Insights into its clinical impact in various types of cancer
TLDR
The main challenge of this review is to discuss the diverse molecular mechanisms for silymarin antiproliferative and apoptotic effects; most of them largely studied in various types of cancers so far.
Silymarin suppresses HepG2 hepatocarcinoma cell progression through downregulation of Slit-2/Robo-1 pathway.
TLDR
Silymarin doses showed anti-carcinogenic, anti-metastatic and apoptotic effects in a dose-dependent manner on HepG2 cells through the Slit-2/Robo-1 pathway.
Silymarin and Cancer: A Dual Strategy in Both in Chemoprevention and Chemosensitivity
TLDR
Silymarin and its derivatives play a double role, namely, limiting the progression of cancer cells through different phases of the cycle and accumulating cancer cells in a phase of the cell cycle—thus making it possible to target a greater number of tumor cells with a specific anticancer agent.
...
1
2
3
4
...

References

SHOWING 1-10 OF 41 REFERENCES
Silibinin inhibits the invasion of human lung cancer cells via decreased productions of urokinase‐plasminogen activator and matrix metalloproteinase‐2
TLDR
It is observed that silibinin exerted a dose‐ and time‐dependent inhibitory effect on the invasion and motility, but hardly on the adhesion, of highly metastatic A549 cells in the absence of cytotoxicity.
Silibinin upregulates the expression of cyclin-dependent kinase inhibitors and causes cell cycle arrest and apoptosis in human colon carcinoma HT-29 cells
TLDR
The results identify molecular mechanisms of silibinin efficacy as a cell cycle regulator and apoptosis inducer in human colon carcinoma HT-29 cells, and justify further studies to investigate potential usefulness of this nontoxic agent in colon cancer prevention and intervention.
Silibinin Inhibits Invasion of Oral Cancer Cells by Suppressing the MAPK Pathway
TLDR
It is suggested that silibinin can reduce the invasion and metastasis of tumor cells, and such a characteristic may be of great value in the development of a potential cancer therapy.
Effects and mechanisms of silibinin on human hepatoma cell lines.
TLDR
It is demonstrated that silibinin significantly reduced the growth of HuH7, HepG2, Hep3B, and PLC/PRF/5 human hepatoma cells and increased acetylation of histone H3 and H4, indicating a possible role of altered histone acetylations in silib inin-reduced HCC cell proliferation.
Silymarin induces apoptosis primarily through a p53-dependent pathway involving Bcl-2/Bax, cytochrome c release, and caspase activation.
TLDR
It is reported that treatment of JB6 C141 cells and p53+/+ fibroblasts with silymarin and silibinin resulted in a dose-dependent inhibition of cell viability and induction of apoptosis in an identical manner and the role of caspase activation in the induction of suicides was suggested.
Silibinin inhibits prostate cancer invasion, motility and migration by suppressing vimentin and MMP-2 expression
TLDR
This study shows that silibinin could inhibit the invasion, motility and migration of ARCaPM cells via down-regulation of vimentin and MMP-2 and therefore may be a promising agent against prostate cancer bone metastasis.
Silymarin Suppresses TNF-Induced Activation of NF-κB, c-Jun N-Terminal Kinase, and Apoptosis
TLDR
The inhibition of activation of NF-κB and the kinases may provide in part the molecular basis for the anticarcinogenic and anti-inflammatory effects of silymarin, and its effects on caspases may explain its role in cytoprotection.
A cancer chemopreventive agent silibinin, targets mitogenic and survival signaling in prostate cancer.
Silymarin suppresses TNF-induced activation of NF-kappa B, c-Jun N-terminal kinase, and apoptosis.
TLDR
The inhibition of activation of NF-kappa B and the kinases may provide in part the molecular basis for the anticarcinogenic and anti-inflammatory effects of silymarin, and its effects on caspases may explain its role in cytoprotection.
...
1
2
3
4
5
...