scholarly journals SOCS2 correlates with malignancy and exerts growth-promoting effects in prostate cancer

2013 ◽  
Vol 21 (2) ◽  
pp. 175-187 ◽  
Author(s):  
Julia Hoefer ◽  
Johann Kern ◽  
Philipp Ofer ◽  
Iris E Eder ◽  
Georg Schäfer ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Expression Patterns ◽  
Mechanistic Explanation ◽  
Tissue Microarrays ◽  
Cytokine Signaling ◽  
Growth Factor Signaling ◽  
Altered Expression

Deregulation of cytokine and growth factor signaling due to an altered expression of endogenous regulators is well recognized in prostate cancer (PCa) and other cancers. Suppressor of cytokine signaling 2 (SOCS2) is a key regulator of the GH, IGF, and prolactin signaling pathways that have been implicated in carcinogenesis. In this study, we evaluated the expression patterns and functional significance of SOCS2 in PCa. Protein expression analysis employing tissue microarrays from two independent patient cohorts revealed a significantly enhanced expression in tumor tissue compared with benign tissue as well as association with Gleason score and disease progression. In vitro and in vivo assays uncovered the involvement of SOCS2 in the regulation of cell growth and apoptosis. Functionally, SOCS2 knockdown inhibited PCa cell proliferation and xenograft growth in a CAM assay. Decreased cell growth after SOCS2 downregulation was associated with cell-cycle arrest and apoptosis. In addition, we proved that SOCS2 expression is significantly elevated upon androgenic stimulation in androgen receptor (AR)-positive cell lines, providing a possible mechanistic explanation for high SOCS2 levels in PCa tissue. Consequently, SOCS2 expression correlated with AR expression in the malignant tissue of patients. On the whole, our study linked increased SOCS2 expression in PCa with a pro-proliferative role in vitro and in vivo.

794: Valproic Acid Inhibits Prostate Cancer Cell Growth in Vitro and in Vivo

2006 ◽  
Vol 175 (4S) ◽  
pp. 257-257
Author(s):  
Jennifer Sung ◽  
Qinghua Xia ◽  
Wasim Chowdhury ◽  
Shabana Shabbeer ◽  
Michael Carducci ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Valproic Acid ◽  
Cell Growth ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Growth

scholarly journals Acetyl-L-Carnitine downregulates invasion (CXCR4/CXCL12, MMP-9) and angiogenesis (VEGF, CXCL8) pathways in prostate cancer cells: rationale for prevention and interception strategies

2019 ◽  
Vol 38 (1) ◽  
Author(s):  
Denisa Baci ◽  
Antonino Bruno ◽  
Caterina Cascini ◽  
Matteo Gallazzi ◽  
Lorenzo Mortara ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Dietary Supplements ◽  
Cell Lines ◽  
Angiogenic Factors ◽  
Migration And Invasion ◽  
Prostate Cancer Cells

Abstract Background Prostate cancer (PCa) is a leading cause of cancer-related death in males worldwide. Exacerbated inflammation and angiogenesis have been largely demonstrated to contribute to PCa progression. Diverse naturally occurring compounds and dietary supplements are endowed with anti-oxidant, anti-inflammatory and anti-angiogenic activities, representing valid compounds to target the aberrant cytokine/chemokine production governing PCa progression and angiogenesis, in a chemopreventive setting. Using mass spectrometry analysis on serum samples of prostate cancer patients, we have previously found higher levels of carnitines in non-cancer individuals, suggesting a protective role. Here we investigated the ability of Acetyl-L-carnitine (ALCAR) to interfere with key functional properties of prostate cancer progression and angiogenesis in vitro and in vivo and identified target molecules modulated by ALCAR. Methods The chemopreventive/angiopreventive activities ALCAR were investigated in vitro on four different prostate cancer (PCa) cell lines (PC-3, DU-145, LNCaP, 22Rv1) and a benign prostatic hyperplasia (BPH) cell line. The effects of ALCAR on the induction of apoptosis and cell cycle arrest were investigated by flow cytometry (FC). Functional analysis of cell adhesion, migration and invasion (Boyden chambers) were performed. ALCAR modulation of surface antigen receptor (chemokines) and intracellular cytokine production was assessed by FC. The release of pro-angiogenic factors was detected by a multiplex immunoassay. The effects of ALCAR on PCa cell growth in vivo was investigated using tumour xenografts. Results We found that ALCAR reduces cell proliferation, induces apoptosis, hinders the production of pro inflammatory cytokines (TNF-α and IFN-γ) and of chemokines CCL2, CXCL12 and receptor CXCR4 involved in the chemotactic axis and impairs the adhesion, migration and invasion capabilities of PCa and BPH cells in vitro. ALCAR exerts angiopreventive activities on PCa by reducing production/release of pro angiogenic factors (VEGF, CXCL8, CCL2, angiogenin) and metalloprotease MMP-9. Exposure of endothelial cells to conditioned media from PCa cells, pre-treated with ALCAR, inhibited the expression of CXCR4, CXCR1, CXCR2 and CCR2 compared to those from untreated cells. Oral administration (drinking water) of ALCAR to mice xenografted with two different PCa cell lines, resulted in reduced tumour cell growth in vivo. Conclusions Our results highlight the capability of ALCAR to down-modulate growth, adhesion, migration and invasion of prostate cancer cells, by reducing the production of several crucial chemokines, cytokines and MMP9. ALCAR is a widely diffused dietary supplements and our findings provide a rational for studying ALCAR as a possible molecule for chemoprevention approaches in subjects at high risk to develop prostate cancer. We propose ALCAR as a new possible “repurposed agent’ for cancer prevention and interception, similar to aspirin, metformin or beta-blockers.

MiR-378 suppresses prostate cancer cell growth through downregulation of MAPK1 in vitro and in vivo

Tumor Biology ◽  
2015 ◽  
Vol 37 (2) ◽  
pp. 2095-2103 ◽  
Author(s):  
Qi-guang Chen ◽  
Wei Zhou ◽  
Tao Han ◽  
Shu-qi Du ◽  
Zhen-hua Li ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Growth

scholarly journals Quercetin inhibits angiogenesis through thrombospondin-1 upregulation to antagonize human prostate cancer PC-3 cell growth in vitro and in vivo

2015 ◽  
Vol 35 (3) ◽  
pp. 1602-1610 ◽  
Author(s):  
FEIYA YANG ◽  
XIAN JIANG ◽  
LIMING SONG ◽  
HUIPING WANG ◽  
ZHU MEI ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Thrombospondin 1

scholarly journals β-arrestin1-medieated inhibition of FOXO3a contributes to prostate cancer cell growth in vitro and in vivo

2018 ◽  
Vol 109 (6) ◽  
pp. 1834-1842 ◽  
Author(s):  
Zhenzhen Kong ◽  
Tuo Deng ◽  
Mengping Zhang ◽  
Zhijian Zhao ◽  
Yang Liu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Growth

CMTM5 is reduced in prostate cancer and inhibits cancer cell growth in vitro and in vivo

2014 ◽  
Vol 17 (6) ◽  
pp. 431-437 ◽  
Author(s):  
Y. Xiao ◽  
Y. Yuan ◽  
Y. Zhang ◽  
J. Li ◽  
Z. Liu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Cancer Cell Growth

Effect of prostatic inhibin peptide (PIP) on prostate cancer cell growth in vitro and in vivo

The Prostate ◽  
1993 ◽  
Vol 22 (3) ◽  
pp. 225-233 ◽  
Author(s):  
Seema Garde ◽  
Anil Sheth ◽  
Arthur T. Porter ◽  
Kenneth J. Pienta
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Growth

scholarly journals Paracrine Insulin-Like Growth Factor Signaling Influences Primordial Germ Cell Migration: In Vivo Evidence from the Zebrafish Model

Endocrinology ◽  
2008 ◽  
Vol 149 (10) ◽  
pp. 5035-5042 ◽  
Author(s):  
Xianpeng Sang ◽  
Matthew S. Curran ◽  
Antony W. Wood
Keyword(s):  
Cell Migration ◽  
Germ Cell ◽  
Zebrafish Embryo ◽  
Expression Patterns ◽  
Primordial Germ Cell ◽  
Growth Factor Signaling ◽  
Zebrafish Model ◽  
Igf Signaling

IGF signaling has been shown to stimulate migration of multiple cell types in vitro, but few studies have confirmed an equivalent function for IGF signaling in vivo. We recently showed that suppression of IGF receptors in the zebrafish embryo disrupts primordial germ cell (PGC) migration, but the mechanism underlying these effects has not been elucidated. We hypothesized that PGCs are intrinsically dependent upon IGF signaling during the migratory phase of development. To test this hypothesis, we first examined the spatial expression patterns of IGF ligand genes (igf1, igf2a, and igf2b) in the zebrafish embryo. In situ analyses revealed distinct expression patterns for each IGF ligand gene, with igf2b mRNA expressed in a spatial pattern that correlates strongly with PGC migration. To determine whether PGC migration is responsive to IGF signaling in vivo, we synthesized gene hybrid expression constructs that permit conditional overexpression of IGF ligands by PGCs into the PGC microenvironment. Conditional overexpression of IGF ligands consistently disrupted PGC migration, confirming that PGC migration is sensitive to local aberrations in IGF signaling. Finally, we show that conditional suppression of IGF signaling, via PGC-specific overexpression of a mutant IGF-I receptor, disrupts PGC migration, confirming that zebrafish PGCs intrinsically require IGF signaling for directional migration in vivo. Collectively, these studies confirm an in vivo role for IGF signaling in cell migration and identify a candidate ligand gene (igf2b) regulating PGC migration in the zebrafish.

scholarly journals AB170. Quercetin inhibits angiogenesis through thrombospondin-1 up-regulation to antagonize human prostate cancer PC-3 cell growth in vitro and in vivo

2016 ◽  
Vol 5 (S1) ◽  
pp. AB170-AB170
Author(s):  
Feiya Yang ◽  
Liming Song ◽  
Nianzeng Xing ◽  
Xian Jiang ◽  
Huiping Wang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Thrombospondin 1

scholarly journals HNRNPM controls circRNA biogenesis and splicing fidelity to sustain cancer cell fitness

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Jessica SY Ho ◽  
Federico Di Tullio ◽  
Megan Schwarz ◽  
Diana Low ◽  
Danny Incarnato ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Solid Tumors ◽  
Cancer Cell ◽  
Antisense Oligonucleotides ◽  
Therapeutic Strategy ◽  
Splicing Factors ◽  
Normal Cells

High spliceosome activity is a dependency for cancer cells, making them more vulnerable to perturbation of the splicing machinery compared to normal cells. To identify splicing factors important for prostate cancer (PCa) fitness, we performed pooled shRNA screens in vitro and in vivo. Our screens identified HNRNPM as a regulator of PCa cell growth. RNA- and eCLIP-sequencing identified HNRNPM binding to transcripts of key homeostatic genes. HNRNPM binding to its targets prevents aberrant exon inclusion and back-splicing events. In both linear and circular mis-spliced transcripts, HNRNPM preferentially binds to GU-rich elements in long flanking proximal introns. Mimicry of HNRNPM dependent linear splicing events using splice-switching-antisense-oligonucleotides (SSOs) was sufficient to inhibit PCa cell growth. This suggests that PCa dependence on HNRNPM is likely a result of mis-splicing of key homeostatic coding and non-coding genes. Our results have further been confirmed in other solid tumors. Taken together, our data reveal a role for HNRNPM in supporting cancer cell fitness. Inhibition of HNRNPM activity is therefore a potential therapeutic strategy in suppressing growth of PCa and other solid tumors.

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