Silibinin Inhibits Cell Growth and Induces Apoptosis through Cell-cycle Arrest in PC-3 Prostate Cancer Cells

김상헌,; 김광연,; 유선녕,; 진영랑,; 전현주,; 이창민,; 안순철,

doi:10.5352/jls.2011.21.11.1573

Cited by 2 publications

(1 citation statement)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, silibinin reduced pro-caspase-3 and increased cleavage form of PARP in a time-dependent manner (Fig. 3b ), as we previously reported [ 32 ]. Next, to identify whether production of mitochondrial ROS by silibinin is associated with apoptosis, we confirmed the change of silibinin-induced apoptosis with the presence or absence of DPI.…”

Section: Resultssupporting

confidence: 87%

Silibinin induces mitochondrial NOX4-mediated endoplasmic reticulum stress response and its subsequent apoptosis

Kim

et al. 2016

BMC Cancer

Self Cite

View full text Add to dashboard Cite

BackgroundSilibinin, a biologically active compound of milk thistle, has chemopreventive effects on cancer cell lines. Recently it was reported that silibinin inhibited tumor growth through activation of the apoptotic signaling pathway. Although various evidences showed multiple signaling pathways of silibinin in apoptosis, there were no reports to address the clear mechanism of ROS-mediated pathway in prostate cancer PC-3 cells. Several studies suggested that reactive oxygen species (ROS) play an important role in various signaling cascades, but the primary source of ROS was currently unclear.MethodsThe effect of silibinin was investigated on cell growth of prostate cell lines by MTT assay. We examined whether silibinin induced apoptosis through production of ROS using flow cytometry. Expression of apoptosis-, endoplasmic reticulum (ER)-related protein and gene were determined by western blotting and RT-PCR, respectively.ResultsResults showed that silibinin triggered mitochondrial ROS production through NOX4 expression and finally led to induce apoptosis. In addition, mitochondrial ROS caused ER stress through disruption of Ca2+ homeostasis. Co-treatment of ROS inhibitor reduced the silibinin-induced apoptosis through the inhibition of NOX4 expression, resulting in reduction of both Ca2+ level and ER stress response.ConclusionsTaken together, silibinin induced mitochondrial ROS-dependent apoptosis through NOX4, which is associated with disruption of Ca2+ homeostasis and ER stress response. Therefore, the regulation of NOX4, mitochondrial ROS producer, could be a potential target for the treatment of prostate cancer.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-016-2516-6) contains supplementary material, which is available to authorized users.

show abstract

Section: Resultssupporting

confidence: 87%

Silibinin induces mitochondrial NOX4-mediated endoplasmic reticulum stress response and its subsequent apoptosis

Kim

et al. 2016

BMC Cancer

Self Cite

View full text Add to dashboard Cite

show abstract

Localization of Translation Initiation Factors to the Postsynaptic Sites

Choi¹,

Park²,

Park³

et al. 2011

Journal of Life Science

View full text Add to dashboard Cite

Local protein synthesis in neuronal dendrites is important for site-specific regulation of synaptic plasticity. In this study, we investigated whether translation initiation factors (eIFs) are present at the postsynaptic sites. High resolution confocal microscopy showed that the eIF4E and eIF4G (which bind the 5'-terminal mRNA cap), eIF5 (which is important during the 3' direction scanning to find an initiation codon), eIF6 (which mediates upregulation of translation by external stimuli), and eIF5A (which mediate translation upregulation under adverse conditions) were localized to the postsynaptic sites. Immunoblot and detergent extraction experiments also indicated that these eIFs were present in the synapse in association with the postsynaptic density (PSD). Our data provide evidence for the strategic positioning of eIFs at the postsynaptic site for initiation of translation in diverse situations.

show abstract

Silibinin Inhibits Cell Growth and Induces Apoptosis through Cell-cycle Arrest in PC-3 Prostate Cancer Cells

Cited by 2 publications

References 32 publications

Silibinin induces mitochondrial NOX4-mediated endoplasmic reticulum stress response and its subsequent apoptosis

Silibinin induces mitochondrial NOX4-mediated endoplasmic reticulum stress response and its subsequent apoptosis

Localization of Translation Initiation Factors to the Postsynaptic Sites

Contact Info

Product

Resources

About