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https://www.readbyqxmd.com/read/28213355/chd1-is-a-synthetic-essential-gene-in-pten-deficient-prostate-cancer
#1
(no author information available yet)
CHD1 is required for the growth of PTEN-deficient prostate cancer cells in vitro and in vivo.
February 17, 2017: Cancer Discovery
https://www.readbyqxmd.com/read/28193700/the-nuclear-transport-receptor-importin-11-is-a-tumor-suppressor-that-maintains-pten-protein
#2
Muhan Chen, Dawid G Nowak, Navneet Narula, Brian Robinson, Kaitlin Watrud, Alexandra Ambrico, Tali M Herzka, Martha E Zeeman, Matthias Minderer, Wu Zheng, Saya H Ebbesen, Kendra S Plafker, Carlos Stahlhut, Victoria M Y Wang, Lorna Wills, Abu Nasar, Mireia Castillo-Martin, Carlos Cordon-Cardo, John E Wilkinson, Scott Powers, Raffaella Sordella, Nasser K Altorki, Vivek Mittal, Brendon M Stiles, Scott M Plafker, Lloyd C Trotman
Phosphatase and tensin homologue (PTEN) protein levels are critical for tumor suppression. However, the search for a recurrent cancer-associated gene alteration that causes PTEN degradation has remained futile. In this study, we show that Importin-11 (Ipo11) is a transport receptor for PTEN that is required to physically separate PTEN from elements of the PTEN degradation machinery. Mechanistically, we find that the E2 ubiquitin-conjugating enzyme and IPO11 cargo, UBE2E1, are limiting factors for PTEN degradation...
February 13, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28191283/active-%C3%AE-catenin-is-regulated-by-the-pten-pi3-kinase-pathway-a-role-for-protein-phosphatase-pp2a
#3
Amit Persad, Geetha Venkateswaran, Li Hao, Maria E Garcia, Jenny Yoon, Jaskiran Sidhu, Sujata Persad
Dysregulation of Wnt/β-catenin signaling has been associated with the development and progression of many cancers. The stability and subcellular localization of β-catenin, a dual functional protein that plays a role in intracellular adhesion and in regulating gene expression, is tightly regulated. However, little is known about the transcriptionally active form of β-catenin, Active Beta Catenin (ABC), that is unphosphorylated at serine 37 (Ser37) and threonine 41 (Thr41). Elucidating the mechanism by which β-catenin is activated to generate ABC is vital to the development of therapeutic strategies to block β-catenin signaling for cancer treatment...
November 2016: Genes & Cancer
https://www.readbyqxmd.com/read/28186998/somatic-molecular-subtyping-of-prostate-tumors-from-hoxb13-g84e-carriers
#4
Tamara L Lotan, Alba Torres, Miao Zhang, Jeffrey J Tosoian, Liana B Guedes, Helen Fedor, Jessica Hicks, Charles M Ewing, Sarah D Isaacs, Dorhyun Johng, Angelo M De Marzo, William B Isaacs
A recurrent germline mutation (G84E) in the HOXB13 gene is associated with early onset and family history-positive prostate cancer in patients of European descent, occurring in up to 5% of prostate cancer families. To date, the molecular features of prostate tumors occurring in HOXB13 G84E carriers have not been studied in a large cohort of patients. We identified 101 heterozygous carriers of G84E who underwent radical prostatectomy for prostate cancer between 1985 and 2011 and matched these men by race, age and tumor grade to 99 HOXB13 wild-type controls...
February 8, 2017: Oncotarget
https://www.readbyqxmd.com/read/28181686/the-effect-of-a-histone-deacetylase-inhibitor-ar-42-on-canine-prostate-cancer-growth-and-metastasis
#5
Said M Elshafae, Nicole A Kohart, Lucas A Altstadt, Wessel P Dirksen, Thomas J Rosol
BACKGROUND: Canine prostate cancer (PCa) is an excellent preclinical model for human PCa. AR-42 is a histone deacetylase inhibitor (HDACi) developed at The Ohio State University that inhibits the proliferation of several cancers, including multiple myeloma, lung, and hepatocellular cancer. In this study, we investigated whether AR-42 would prevent or decrease. The growth and metastasis of a canine PCa (Ace-1 cells) to bone in vitro and in vivo. METHODS: Proliferation, cell viability, invasion, and metastasis of a canine prostate cancer cell line (Ace-1) were measured following treatment with AR-42...
February 9, 2017: Prostate
https://www.readbyqxmd.com/read/28178391/amino-terminal-enhancer-of-split-gene-aes-encodes-a-tumor-and-metastasis-suppressor-of-prostate-cancer
#6
Yoshiyuki Okada, Masahiro Sonoshita, Fumihiko Kakizaki, Naoki Aoyama, Yoshiro Itatani, Masayuki Uegaki, Hiromasa Sakamoto, Takashi Kobayashi, Takahiro Inoue, Tomomi Kamba, Akira Suzuki, Osamu Ogawa, M Mark Taketo
Major cause of cancer death is its metastasis to the vital organs. Few effective therapies are available for metastatic castration-resistant prostate cancer (PCa), and progressive metastatic lesions such as lymph nodes and bones cause mortality. We recently identified AES as a metastasis suppressor for colon cancer. Here, we have studied the roles of AES in PCa progression. We analyzed the relationship between AES expression and PCa stages of progression by immunohistochemistry of human needle biopsy samples...
February 8, 2017: Cancer Science
https://www.readbyqxmd.com/read/28166537/synthetic-essentiality-of-chromatin-remodelling-factor-chd1-in-pten-deficient-cancer
#7
Di Zhao, Xin Lu, Guocan Wang, Zhengdao Lan, Wenting Liao, Jun Li, Xin Liang, Jasper Robin Chen, Sagar Shah, Xiaoying Shang, Ming Tang, Pingna Deng, Prasenjit Dey, Deepavali Chakravarti, Peiwen Chen, Denise J Spring, Nora M Navone, Patricia Troncoso, Jianhua Zhang, Y Alan Wang, Ronald A DePinho
Synthetic lethality and collateral lethality are two well-validated conceptual strategies for identifying therapeutic targets in cancers with tumour-suppressor gene deletions. Here, we explore an approach to identify potential synthetic-lethal interactions by screening mutually exclusive deletion patterns in cancer genomes. We sought to identify 'synthetic-essential' genes: those that are occasionally deleted in some cancers but are almost always retained in the context of a specific tumour-suppressor deficiency...
February 6, 2017: Nature
https://www.readbyqxmd.com/read/28156002/lucap-prostate-cancer-patient-derived-xenografts-reflect-the-molecular-heterogeneity-of-advanced-disease-an-d-serve-as-models-for-evaluating-cancer-therapeutics
#8
Holly M Nguyen, Robert L Vessella, Colm Morrissey, Lisha G Brown, Ilsa M Coleman, Celestia S Higano, Elahe A Mostaghel, Xiaotun Zhang, Lawrence D True, Hung-Ming Lam, Martine Roudier, Paul H Lange, Peter S Nelson, Eva Corey
BACKGROUND: Metastatic prostate cancer is a common and lethal disease for which there are no therapies that produce cures or long-term durable remissions. Clinically relevant preclinical models are needed to increase our understanding of biology of this malignancy and to evaluate new agents that might provide effective treatment. Our objective was to establish and characterize patient-derived xenografts (PDXs) from advanced prostate cancer (PC) for investigation of biology and evaluation of new treatment modalities...
February 3, 2017: Prostate
https://www.readbyqxmd.com/read/28152502/methylation-decreases-the-bin1-tumor-suppressor-in-escc-and-restoration-by-decitabine-inhibits-the-epithelial-mesenchymal-transition
#9
Xuexiao Wang, Jiali Wang, Yunlong Jia, Yu Wang, Xiaonan Han, Yuqing Duan, Wei Lv, Ming Ma, Lihua Liu
Bridging integrator-1 (Bin1), as a tumor suppressor, is frequently attenuated or even abolished in multiple primary cancers. A reduced expression of Bin1 caused by DNA methylation, has been reported in breast and prostate cancers. However, the methylation status of Bin1 and potent biological functions in esophageal squamous cell carcinoma (ESCC) remain unclear. In a previous study, we showed that the Bin1 expression was low in ESCC tissues. Herein, we further characterized this mechanism, confirming that gene hypermethylation was significantly correlated with the aberrant attenuation of Bin1...
January 31, 2017: Oncotarget
https://www.readbyqxmd.com/read/28146062/high-level-%C3%AE-glutamyl-hydrolase-ggh-expression-is-linked-to-poor-prognosis-in-erg-negative-prostate-cancer
#10
Nathaniel Melling, Masoud Rashed, Cornelia Schroeder, Claudia Hube-Magg, Martina Kluth, Dagmar Lang, Ronald Simon, Christina Möller-Koop, Stefan Steurer, Guido Sauter, Frank Jacobsen, Franziska Büscheck, Corinna Wittmer, Till Clauditz, Till Krech, Maria Christina Tsourlakis, Sarah Minner, Hartwig Huland, Markus Graefen, Lars Budäus, Imke Thederan, Georg Salomon, Thorsten Schlomm, Waldemar Wilczak
γ-glutamyl-hydrolase (GGH) is a ubiquitously-expressed enzyme that regulates intracellular folate metabolism for cell proliferation, DNA synthesis, and repair. Employing GGH immunohistochemistry on a tissue microarray with 12,427 prostate cancers, we found that GGH expression was negative to low in normal prostate epithelium, whereas 88.3% of our 10,562 interpretable cancers showed GGH expression. GGH staining was considered as low intensity in 49.6% and as high intensity in 38.6% of cancers. High GGH expression was linked to the TMPRSS2:ERG-fusion positive subset of cancers (p < 0...
January 29, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28124475/genome-wide-two-locus-interaction-analysis-identifies-multiple-epistatic-snp-pairs-that-confer-risk-of-prostate-cancer-a-cross-population-study
#11
Jiawei Shen, Zhiqiang Li, Zhijian Song, Jianhua Chen, Yongyong Shi
Prostate cancer is one of the most common carcinomas among adult males. Recently, genome-wide association studies (GWAS) have identified several susceptibility genes of prostate cancer. However, these single locus results can only explain a small proportion of the genetic etiology. In order to understand how multiple genetics variants may contribute to the penetrance of prostate cancer, we conducted a genome-wide SNP-SNP interaction study in four populations, involving 5,269 cases and 5,289 controls. We exhaustively evaluated all pairs of SNP-SNP interactions for 661,658 SNPs that were consensus in all four groups, and then performed a meta-analysis to combine the results...
January 25, 2017: International Journal of Cancer. Journal International du Cancer
https://www.readbyqxmd.com/read/28112153/dissecting-cell-type-specific-roles-of-androgen-receptor-in-prostate-homeostasis-and-regeneration-through-lineage-tracing
#12
Qing Xie, Yueli Liu, Tao Cai, Corrigan Horton, Joshua Stefanson, Zhu A Wang
Androgen signals through androgen receptor (AR) to influence prostate development and cancer. How stromal and epithelial AR regulate prostate homeostasis remains unclear. Using genetic lineage tracing, we systematically investigated the role of cell-autonomous AR in different prostate epithelial cell types. Here we show that AR is dispensable for basal cell maintenance, but is cell-autonomously required for the luminal differentiation of rare basal stem cells. In contrast, AR deletion in luminal cells alters cell morphology and induces transient over-proliferation, without affecting androgen-mediated luminal cell survival or regeneration...
January 23, 2017: Nature Communications
https://www.readbyqxmd.com/read/28107872/mir-21-targets-and-inhibits-tumor-suppressor-gene-pten-to-promote-prostate-cancer-cell-proliferation-and-invasion-an-experimental-study
#13
Yu Yang, Jia-Xiang Guo, Zhi-Qiang Shao
OBJECTIVE: To study whether miR-21 targets and inhibits tumor suppressor gene PTEN can promote prostate cancer cell proliferation and invasion. METHODS: Prostate cancer cell lines PC-3 were cultured and divided into negative control group (NC group), miR-21 group, pcDNA3.1 group, miR-21+pcDNA3.1 group and miR-21+PTEN group that were transfected with different miR and plasmid, respectively. After 12 h and 24 h of transfection, the cell viability and invasive cell number were determined; after 24 h of transfection, Bcl-2, Survivin, MMP2, MMP9, PTEN, PI3K, and AKT expression in cells were determined...
January 2017: Asian Pacific Journal of Tropical Medicine
https://www.readbyqxmd.com/read/28106991/discovery-of-a-phosphoinositide-3-kinase-pi3k-b-d-inhibitor-for-the-treatment-of-phosphatase-and-tensin-homolog-pten-deficient-tumors-building-pi3kb-potency-in-a-pi3kd-selective-template-by-targeting-non-conserved-asp856
#14
Stéphane Perreault, Jayaraman Chandrasekhar, Zhi-Hua Cui, Jerry B Evarts, Jia Hao, Joshua A Kaplan, Adam Kashishian, Kathleen S Keegan, Thomas Kenney, David J Koditek, Latesh Lad, Eve-Irene Lepist, Mary E McGrath, Leena Patel, Bart Phillips, Joseph Therrien, Jennifer Treiberg, Anella Yahiaoui, Gary Phillips
Phosphoinositide 3-kinase (PI3K) beta signaling is required to sustain cancer cell growth in which the tumor suppressor phosphatase and tensin homolog (PTEN) has been deactivated. This manuscript describes the discovery, optimization, and in vivo evaluation of a novel series of PI3Kbeta/delta inhibitors in which PI3Kbeta potency was built in a PI3Kdelta-selective template. This work led to the discovery of a highly selective PI3Kbeta/delta inhibitor displaying excellent pharmacokinetic profile and efficacy in a human PTEN-deficient LNCaP prostate carcinoma xenograft tumor model...
January 20, 2017: Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/28059767/rb1-and-trp53-cooperate-to-suppress-prostate-cancer-lineage-plasticity-metastasis-and-antiandrogen-resistance
#15
Sheng Yu Ku, Spencer Rosario, Yanqing Wang, Ping Mu, Mukund Seshadri, Zachary W Goodrich, Maxwell M Goodrich, David P Labbé, Eduardo Cortes Gomez, Jianmin Wang, Henry W Long, Bo Xu, Myles Brown, Massimo Loda, Charles L Sawyers, Leigh Ellis, David W Goodrich
Prostate cancer relapsing from antiandrogen therapies can exhibit variant histology with altered lineage marker expression, suggesting that lineage plasticity facilitates therapeutic resistance. The mechanisms underlying prostate cancer lineage plasticity are incompletely understood. Studying mouse models, we demonstrate that Rb1 loss facilitates lineage plasticity and metastasis of prostate adenocarcinoma initiated by Pten mutation. Additional loss of Trp53 causes resistance to antiandrogen therapy. Gene expression profiling indicates that mouse tumors resemble human prostate cancer neuroendocrine variants; both mouse and human tumors exhibit increased expression of epigenetic reprogramming factors such as Ezh2 and Sox2...
January 6, 2017: Science
https://www.readbyqxmd.com/read/28057891/prostate-cancer-pi3k-pten-and-prognosis
#16
REVIEW
Helen M Wise, Miguel A Hermida, Nicholas R Leslie
Loss of function of the PTEN tumour suppressor, resulting in dysregulated activation of the phosphoinositide 3-kinase (PI3K) signalling network, is recognized as one of the most common driving events in prostate cancer development. The observed mechanisms of PTEN loss are diverse, but both homozygous and heterozygous genomic deletions including PTEN are frequent, and often accompanied by loss of detectable protein as assessed by immunohistochemistry (IHC). The occurrence of PTEN loss is highest in aggressive metastatic disease and this has driven the development of PTEN as a prognostic biomarker, either alone or in combination with other factors, to distinguish indolent tumours from those likely to progress...
February 1, 2017: Clinical Science (1979-)
https://www.readbyqxmd.com/read/28009609/atypical-intraductal-cribriform-proliferations-of-the-prostate-exhibit-similar-molecular-and-clinicopathologic-characteristics-as-intraductal-carcinoma-of-the-prostate
#17
Richard A Hickman, Hui Yu, Jianhong Li, Max Kong, Rajal B Shah, Ming Zhou, Jonathan Melamed, Fang-Ming Deng
Atypical intraductal cribriform proliferations of the prostate (AIP) are loose cribriform proliferations of luminal cells that exhibit greater architectural complexity and/or nuclear atypia than high-grade prostatic intraepithelial neoplasia (HGPIN), but lack the diagnostic criteria for intraductal carcinoma (IDC). The significance of AIP has not been formally established. We compared the clinical, morphologic, and immunohistochemical characteristics of AIP with classic IDC in 310 radical prostatectomy specimens that were received over an 18-month period...
December 22, 2016: American Journal of Surgical Pathology
https://www.readbyqxmd.com/read/27995550/somatic-mutations-in-prostate-cancer-closer-to-personalized-medicine
#18
REVIEW
M J Alvarez-Cubero, L J Martinez-Gonzalez, I Robles-Fernandez, J Martinez-Herrera, G Garcia-Rodriguez, M Pascual-Geler, J M Cozar, J A Lorente
The molecular cause of prostate cancer (PCa) is still unclear; however, its progression involves androgen, PI3K/Akt, and PTEN signaling, as cycle and apoptotic pathways. Alterations in oncogenes and tumor suppressor genes as PIK3CA, BRAF, KRAS and TP53 are not very common. Recently, somatic mutations have been discovered in relation to cancer progression mainly in genes such as PIK3CA; however, little data has been described in PCa. Nowadays genetic tools allow us to investigate multiple details about the biological heterogeneity of PCa, to better understand the mechanisms of disease progression and treatment resistance...
December 19, 2016: Molecular Diagnosis & Therapy
https://www.readbyqxmd.com/read/27955654/depletion-of-sag-rbx2-e3-ubiquitin-ligase-suppresses-prostate-tumorigenesis-via-inactivation-of-the-pi3k-akt-mtor-axis
#19
Mingjia Tan, Jie Xu, Javed Siddiqui, Felix Feng, Yi Sun
BACKGROUND: SAG (Sensitive to Apoptosis Gene), also known as RBX2, ROC2 or RNF7, is a RING component of CRL (Cullin-RING ligase), required for its activity. Our recent study showed that SAG/RBX2 co-operated with Kras to promote lung tumorigenesis, but antagonized Kras to inhibit skin tumorigenesis, suggesting a tissue/context dependent function of Sag. However, it is totally unknown whether and how Sag would play in prostate tumorigenesis, triggered by Pten loss. METHODS: Sag and Pten double conditional knockout mice were generated and prostate specific deletion of Sag and Pten was achieved by PB4-Cre, and their effect on prostate tumorigenesis was evaluated by H&E staining...
December 12, 2016: Molecular Cancer
https://www.readbyqxmd.com/read/27941799/inhibition-of-notch-pathway-arrests-pten-deficient-advanced-prostate-cancer-by-triggering-p27-driven-cellular-senescence
#20
Ajinkya Revandkar, Maria Luna Perciato, Alberto Toso, Abdullah Alajati, Jingjing Chen, Hermeto Gerber, Mitko Dimitrov, Andrea Rinaldi, Nicolas Delaleu, Emiliano Pasquini, Rocco D'Antuono, Sandra Pinton, Marco Losa, Letizia Gnetti, Alberto Arribas, Patrick Fraering, Francesco Bertoni, Alain Nepveu, Andrea Alimonti
Activation of NOTCH signalling is associated with advanced prostate cancer and treatment resistance in prostate cancer patients. However, the mechanism that drives NOTCH activation in prostate cancer remains still elusive. Moreover, preclinical evidence of the therapeutic efficacy of NOTCH inhibitors in prostate cancer is lacking. Here, we provide evidence that PTEN loss in prostate tumours upregulates the expression of ADAM17, thereby activating NOTCH signalling. Using prostate conditional inactivation of both Pten and Notch1 along with preclinical trials carried out in Pten-null prostate conditional mouse models, we demonstrate that Pten-deficient prostate tumours are addicted to the NOTCH signalling...
December 12, 2016: Nature Communications
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