Qianliening capsule treats benign prostatic hyperplasia via suppression of the EGF/STAT3 signaling pathway

Lin, Jiumao; Zhou, Jianheng; Xu, Wei; Zhong, Xiaoyong; Zhang, Hong; Peng, Jun

doi:10.3892/etm.2013.1008

Cited by 17 publications

(21 citation statements)

References 22 publications

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“…Previous studies have demonstrated that EGF stimulates STAT3 activation, which upregulates the levels of phosphorylated STAT3 in BPH prostatic cells (16)(17)(18)(19)(20). Therefore, in the present study, STAT3 activation in WPMY-1 cells was stimulated with EGF.…”

Section: Qc Inhibits the Activation Of The Stat3 Signaling Pathway Inmentioning

confidence: 63%

“…The signal transducer and activator of transcription 3 (STAT3) pathway is one of the main growth factor-mediated signal transduction pathways and is closely associated with the occurrence of BPH (13)(14)(15). Abnormal activation of the pathway can lead to a significant increase in the expression levels of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) and the pro-proliferative protein cyclin D1, which in turn promote cell growth and the inhibition of apoptosis, which leads to the abnormal proliferation and malignant transformation of cells (16).…”

Section: Introductionmentioning

confidence: 99%

“…Epidermal growth factor (EGF) is an important factor in the promotion of mitosis and proliferation. Studies have demonstrated that EGF has an important effect on prostate growth and its abnormal expression is a key factor in BPH (16)(17)(18). EGF elicits its biological effects through binding to its receptor (EGFR).…”

Section: Introductionmentioning

confidence: 99%

“…EGF elicits its biological effects through binding to its receptor (EGFR). Upon interaction with EGF, the EGFR induces the phosphorylation/activation of STAT3, a transcription factor essential for cell survival and proliferation (16,19,20). The phosphorylation of STAT3 in the cytoplasm induces its homodimerization, nuclear translocation and DNA binding, resulting in the expression of various essential genes involved in cell proliferation and survival (21)(22)(23)(24).…”

Section: Introductionmentioning

confidence: 99%

“…In addition, studies involving animal experiments have demonstrated that QC significantly decreases the prostatic volume and weight and inhibits prostatic hyperplasia. Previous studies by our group have shown that this occurs by improving the abnormal ratio of estrogen to androgen in the serum via regulating the expression of estrogen receptor (ER) and androgen receptor (AR) (30), inhibiting the expression levels of pro-proliferative cyclin D1, proliferating cell nuclear antigen and cyclin-dependent kinase 4 (CDK4) via suppression of the EGF/STAT3 signaling pathway in vivo (16), and inducing prostatic cell apoptosis through the mitochondrion-dependent apoptotic pathway in vivo and in vitro (32,33). However, the precise mechanism of its anti-BPH activity remains to be fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of the signal transducer and activator of transcription 3 signaling pathway by Qianliening capsules suppresses the growth and induces the apoptosis of human prostate cells

Lin

Zhou

Zhong

et al. 2014

Molecular Medicine Reports

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The signal transducer and activator of transcription 3 (STAT3) pathway is one of the main growth factor-mediated signal transduction pathways and is closely associated with the occurrence and development of benign prostatic hyperplasia (BPH). Qianliening capsules (QC) have significant therapeutic effects on BPH; however, the precise mechanism underlying its anti-BPH activity remains to be elucidated. To further elucidate the molecular mechanism of the therapeutic effect of QC on BPH, the present study used epidermal growth factor (EGF), which has a role in the pathogenesis of BPH, to stimulate the growth of human prostate WPMY-1 cells and activate the STAT3 pathway in the WPMY-1 cells. The cell viability was determined using an MTT assay and the cell morphology was observed by phase-contrast microscopy. Fluorescence activated cell sorting analysis with Annexin-V/propidium iodide (PI) staining and PI staining were performed to examine cell apoptosis and the cell cycle. The activation of caspase-9 and -3 were evaluated by colorimetric assay. STAT3 phosphorylation and transcriptional activity were detected by western blot analysis and the luciferase gene reporter, respectively. The mRNA and protein expression levels of B-cell lymhoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), cyclin D1, cyclin-dependent kinase 4 (CDK4) and p21 were measured by reverse transcription quantitative polymerase chain reaction and western blot analysis, respectively. In the present study, QC was found to significantly and dose-dependently inhibit the EGF-stimulated growth of WPMY-1 cells, as evidenced by QC-induced cell morphological changes and a reduction in cell viability. In addition, QC treatment markedly induced the activation of caspase-9 and -3. QC treatment also inhibited the EGF-mediated increase of STAT3 phosphorylation levels and transcriptional activity in WPMY-19 cells, accompanied by downregulation of the expression of Bcl-2, cyclin D1 and CDK4 and upregulation of the expression of Bax and p21. These results suggested that QC effectively inhibited the proliferation and promoted the apoptosis of human prostate cells via modulation of the STAT3 signaling pathway and its target genes, which is likely to be one of the mechanisms underlying its activity in BPH treatment.

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Section: Qc Inhibits the Activation Of The Stat3 Signaling Pathway Inmentioning

confidence: 63%