scholarly journals MiR-455-5p Suppresses the Progression of Prostate Cancer by Targeting CCR5

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Qianwei Xing ◽  
Huyang Xie ◽  
Bingye Zhu ◽  
Zhiwei Sun ◽  
Yeqing Huang
Keyword(s):  
Prostate Cancer ◽  
Chemokine Receptor ◽  
Poor Prognosis ◽  
Therapeutic Strategy ◽  
Caspase 3 ◽  
Cellular Proliferation ◽  
Cancer Center ◽  
Human Prostate Cancer ◽  
Inhibit Tumor Growth ◽  
Functional Assays

Accumulated evidence indicates that miR-455-5p functions as tumor suppressor in the progression of various cancers. However, the mechanism through which miR-455-5p influences the tumorigenesis of human prostate cancer (PCa) remains undetermined. In this study, reanalysis of data obtained from the Memorial Sloan Kettering Cancer Center showed that miR-455-5p can be used as biomarker for PCa diagnosis and predictor of poor prognosis. Functional assays indicated that miR-455-5p overexpression could suppress cellular proliferation, inhibit tumor growth, and trigger apoptosis by activating and cleaving caspase 3. We experimentally verified that miR-455-5p negatively regulated the C–C motif chemokine receptor 5 (CCR5). Overall, our data demonstrate that miR-455-5p suppressed PCa cellular proliferation and induced cell apoptosis by downregulating CCR5. Thus, miR-455-5p may be considered a new therapeutic strategy for PCa.

1495: Elevated Expression of Tumor-Associated Macrophages is Associated with Poor Prognosis of Human Prostate Cancer

2006 ◽  
Vol 175 (4S) ◽  
pp. 483-483
Author(s):  
Hitoshi Takayama ◽  
Norio Nonomura ◽  
Daizo Oka ◽  
Masahiro Shiba ◽  
Yasuyuki Arai ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Poor Prognosis ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Tumor Associated Macrophages ◽  
Elevated Expression

scholarly journals Supercritical Fluid Extraction of Citrus iyo Hort. ex Tanaka Pericarp Inhibits Growth and Induces Apoptosis Through Abrogation of STAT3 Regulated Gene Products in Human Prostate Cancer Xenograft Mouse Model

2016 ◽  
Vol 16 (2) ◽  
pp. 227-243 ◽  
Author(s):  
Chulwon Kim ◽  
Il Ho Lee ◽  
Ho Bong Hyun ◽  
Jong-Chan Kim ◽  
Rajendra Gyawali ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Cellular Proliferation ◽  
Human Prostate ◽  
Parp Cleavage ◽  
G1 Arrest ◽  
Gene Products ◽  
Human Prostate Cancer ◽  
Male Mice

Activation of signal transducer and activator of transcription 3 (STAT3) is well known to play a major role in the cell growth, survival, proliferation, metastasis, and angiogenesis of various cancer cells. Most of the citrus species offer large quantities of phytochemicals that have beneficial effects attributed to their chemical components. Our study was carried out to evaluate the anticancer effects of the pericarp of Iyokan ( Citrus iyo Hort. ex Tanaka), locally known as yeagam in Korea, through modulation of the STAT3 signaling pathway in both tumor cells and a nude mice model. The effect of supercritical extracts of yeagam peel (SEYG) on STAT3 activation, associated protein kinases, STAT3-regulated gene products, cellular proliferation, and apoptosis was examined. The in vivo effect of SEYG on the growth of DU145 human prostate xenograft tumors in athymic nu/nu male mice was also investigated. We found SEYG exerted substantial inhibitory effect on STAT3 activation in human prostate cancer DU145 cells as compared to other tumor cells analyzed. SEYG inhibited proliferation and downregulated the expression of various STAT3-regulated gene products such as bcl-2, bcl-xL, survivin, IAP-1/2, cyclin D1, cyclin E, COX-2, VEGF, and MMP-9. This correlated with an increase in apoptosis as indicated by an increase in the expression of p53 and p21 proteins, the sub-G1 arrest, and caspase-3-induced PARP cleavage. When administered intraperitoneally, SEYG reduced the growth of DU145 human prostate xenograft tumors through downmodulation of STAT3 activation in athymic nu/nu male mice. Overall, these results suggest that SEYG extract has the potential source of STAT3 inhibitors that may have a potential in chemoprevention of human prostate cancer cells.

scholarly journals Inhibition of Prostate Cancer Cell Growth by Human Secreted PDZ Domain-Containing Protein 2, a Potential Autocrine Prostate Tumor Suppressor

Endocrinology ◽  
2006 ◽  
Vol 147 (11) ◽  
pp. 5023-5033 ◽  
Author(s):  
C. W. Tam ◽  
A. S. Cheng ◽  
R. Y. M. Ma ◽  
K.-M. Yao ◽  
S. Y. W. Shiu
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Pdz Domain ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Lncap Cells ◽  
Prostate Cancer Cells ◽  
Autocrine Growth ◽  
Endogenous Expression

A possible role of the PDZ domain-containing protein 2 (PDZD2) in prostate tumorigenesis has been suggested. Besides, PDZD2 is posttranslationally cleaved by a caspase-dependent mechanism to form a secreted PDZ domain-containing protein 2 (sPDZD2) with unknown functions in humans. In this study, we demonstrate the endogenous expression of PDZD2 and secretion of sPDZD2 in cancerous DU145, PC-3, 22Rv1, LNCaP, and immortalized RWPE-1 prostate epithelial cells. Inhibition of endogenous sPDZD2 production and secretion by DU145, PC-3, 22Rv1, and RWPE-1 cells via the caspase-3 inhibitor Z-DEVD-FMK resulted in increased cell proliferation, which was abrogated by treatment with exogenous recombinant sPDZD2. Whereas sPDZD2-induced antiproliferation in DU145, PC-3, and 22Rv1 cells, it induced apoptosis in LNCaP cells. The data suggest that endogenous sPDZD2, produced by caspase-3-mediated cleavage from PDZD2, may function as a novel autocrine growth suppressor for human prostate cancer cells. The antiproliferative effect of sPDZD2 was apparently mediated through slowing the entry of DU145, PC-3, and 22Rv1 cells into the S phase of the cell cycle. In DU145 cells, this can be attributed to stimulated p53 and p21CIP1/WAF1 expression by sPDZD2. On the other hand, the apoptotic effect of sPDZD2 on LNCaP cells was apparently mediated via p53-independent Bad stimulation. Together our results indicate the presence of p53-dependent and p53-independent PDZD2/sPDZD2 autocrine growth suppressive signaling pathways in human prostate cancer cells and suggest a novel therapeutic approach of harnessing the latent tumor-suppressive potential of an endogenous autocrine signaling protein like sPDZD2 to inhibit prostate cancer growth.

scholarly journals Ethyl Acetate Extracts of Semen Impatientis Inhibit Proliferation and Induce Apoptosis of Human Prostate Cancer Cell Lines through AKT/ERK Pathways

2017 ◽  
Vol 2017 ◽  
pp. 1-9
Author(s):  
Tao Wang ◽  
Yang Cai ◽  
Wen Song ◽  
Ruibao Chen ◽  
Dunmei Hu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Western Blot ◽  
Ethyl Acetate ◽  
Caspase 3 ◽  
Inhibitory Effect ◽  
G1 Phase ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Impatiens Balsamina ◽  
Ethyl Acetate Extracts

Objective. To investigate the inhibitory effect of ethyl acetate extracts of Impatiens balsamina L. on prostate cancer cells. Methods. Impatiens balsamina L. was extracted to get water, ethanol, oil ether, ethyl acetate, and butanol extracts. CCK-8 assay was used to detect the inhibitory effect. Apoptosis rates and cell cycle distribution were detected by flow cytometry. Transwell assay was performed to test the ability of migration. The expressions of Bcl-2, Bax, cleaved-caspase-3, p-ERK, ERK, p-AKT, AKT, cyclin D1, cyclin E, and MMP2 were detected by Western blot. Results. Ethyl acetate extracts had the strongest inhibitory effect. After being treated with different concentrations of ethyl acetate extracts, the percentage of G0/G1 phase increased significantly, cyclin D1 and cyclin E expression decreased, apoptosis rate was significantly higher, and the ability of migration of PC-3 and RV1 was inhibited significantly. Western blot showed that the expressions of Bcl-2, p-ERK, and p-AKT were significantly decreased, but the expressions of Bax and caspase-3 cleavage were increased. Conclusions. Impatiens balsamina L. inhibited the proliferation of human prostate cancer cells; ethyl acetate extracts have the strongest effect. It could inhibit cell proliferation and migration, cause G1 phase arrest, and induce apoptosis probably through inhibition of the AKT and ERK pathways.

scholarly journals Independence of HIF1a and androgen signaling pathways in prostate cancer

2019 ◽  
Author(s):  
Maxine GB Tran ◽  
Becky AS Bibby ◽  
Lingjian Yang ◽  
Franklin Lo ◽  
Anne Warren ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Growth ◽  
Signaling Pathways ◽  
Cancer Progression ◽  
Poor Prognosis ◽  
Therapeutic Strategy ◽  
Promote Tumor Growth ◽  
Elevated Expression

AbstractAndrogen signaling drives prostate cancer progression and is a therapeutic target. Hypoxia/HIF1a signaling is associated with resistance to hormone therapy and a poor prognosis in patients treated with surgery or radiotherapy. It is not known whether the pathways operate in cooperation or independently. Using LNCaP cells with and without stable transfection of a HIF1a expression vector, we show that combined AR and HIF1a signaling promotes tumor growth in vitro and in vivo, and the capacity of HIF1a to promote tumor growth in the absence of endogenous androgen in vivo. Gene expression analysis identified 7 genes that were upregulated by both androgen and HIF1a. ChIP-Seq analysis showed that the AR and HIF/hypoxia signaling pathways function independently regulating the transcription of different genes with few shared targets. In clinical datasets elevated expression of 5 of the 7 genes was associated with a poor prognosis. Our findings suggest that simultaneous therapeutic inhibition of AR and HIF1a signaling pathways should be explored as a potential therapeutic strategy.

scholarly journals The Effect of Ethanol Baneh Skin Extract on the Expressions of Bcl - 2, Bax, and Caspase - 3 Concentration in Human Prostate Cancer pc3 Cells

2018 ◽  
Vol 11 (3) ◽  
Author(s):  
Maryam Amiri ◽  
Foad Nasrollahi ◽  
Siamak Barghi ◽  
Nazanin Ebrahimi ◽  
Afsaneh Rajizadeh ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Caspase 3 ◽  
Human Prostate ◽  
Skin Extract ◽  
Human Prostate Cancer ◽  
Pc3 Cells

Physiologically Attainable Concentrations of Lycopene Induce Mitochondrial Apoptosis in LNCaP Human Prostate Cancer Cells

2005 ◽  
Vol 230 (3) ◽  
pp. 171-179 ◽  
Author(s):  
Holly L. Hantz ◽  
Leeanne F. Young ◽  
Keith R. Martin
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Mitochondrial Function ◽  
Cellular Proliferation ◽  
The United States ◽  
Human Prostate ◽  
Brdu Incorporation ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Trypan Blue Exclusion

Prostate cancer is the second leading cause of cancer deaths among men in the United States. Studies show that people with diets rich in tomato-based foods have reduced risks of cancer, viz., prostate cancer. This is attributed, in part, to lycopene, the most abundant carotenoid in tomatoes. Thus, we studied the effect of lycopene at physiologically attainable concentrations on apoptosis, cellular proliferation, and necrosis in LNCaP human prostate cancer cells. Cells at 37°C and >80% confluency were treated with media alone (0.32% tetrahydrofuran vehicle) or with increasing concentrations (0.3–3.0 μM) of lycopene overnight. After washing monolayers, analyses by high-performance liquid chromatography (HPLC) showed that cellular accumulation of lycopene was 5.5 ± 0.8, 14.0 ± 3.2, and 36.7 ± 12.3 pmole/106 cells for 0.3, 1.0, and 3.0 μM, respectively, and not detected in control cells. Lycopene did not alter cellular proliferation because bromodeoxyuridine (BrdU) incorporation and cell numbers were identical among groups. However, results of a 3[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay showed that mitochondrial function decreased 61%–83% with increasing concentrations of lycopene (P < 0.001). Cytotoxicity and necrosis did not contribute to this effect because lactate dehydrogenase (LDH) release (1.5%–1.8%) and trypan blue exclusion (89%–93%) were similar. Subsequently, we demonstrated that increasing concentrations of lycopene significantly (P < 0.05) reduced mitochondrial transmembrane potential, induced the release of mitochondrial cytochrome c, and increased annexin V binding, confirming induction of apoptosis. Thus, lycopene at physiologically relevant concentrations did not affect cellular proliferation or promote necrosis but clearly altered mitochondrial function and induced apoptosis in LNCaP human prostate cancer cells.

Sign in / Sign up

Export Citation Format

Share Document