• Filter By:
• Specialty
• Source
• Condition
• Cancer
• Infectious Disease
• Drug
• Training
• Management
• Procedure
• Therapy
• Vaccine
• Nutrition
• Country

Radiosensitization by the investigational NEDD8-activating enzyme inhibitor MLN4924 (pevonedistat) in hormone-resistant prostate cancer cells.
Authors: Wang X, Zhang W, Yan Z, Liang Y, Li L, Yu X, Feng Y, Fu S, Zhang Y, Zhao H, Yu J, Jeong LS, Guo X, Jia L Abstract Salvage radiotherapy (SRT) is the first-line treatment for prostate cancer patients with biochemical recurrence following radical prostatectomy, and new specific radiosensitizers are in urgent need to enhance SRT effect. MLN4924 (also known as Pevonedistat), a specific inhibitor of NEDD8-activating enzyme, has recently entered phase I/II clinical trials in several malignancies. By inhibiting cullin neddylation, MLN4924 inactivates Cullin-RING ligases (CRL), which have been validated as an attra...
Source: Oncotarget - May 27, 2016 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Phosphoproteomic analysis identifies FAK2 as a potential therapeutic target for tamoxifen resistance in breast cancer.
Abstract Tamoxifen, an estrogen receptor-α (ER) antagonist, is an important agent for the treatment of breast cancer. However, this therapy is complicated by the fact that a substantial number of patients exhibit either de novo or acquired resistance. To characterize the signaling mechanisms underlying this resistance, we treated the MCF7 breast cancer cell line with tamoxifen for over six months and showed that this cell line acquired resistance to tamoxifen in vitro and in vivo. We performed SILAC-based quantitative phosphoproteomic profiling on the tamoxifen resistant and vehicle-treated sensitive cell lines t...
Source: Molecular and Cellular Proteomics : MCP - September 1, 2015 Category: Molecular Biology Authors: Wu X, Zahari MS, Renuse S, Nirujogi RS, Kim MS, Manda SS, Stearns V, Gabrielson E, Sukumar S, Pandey A Tags: Mol Cell Proteomics Source Type: research

Endoplasmic reticulum Ca(2+) content decrease by PKA-dependent hyperphosphorylation of type 1 IP3 receptor contributes to prostate cancer cell resistance to androgen deprivation.
Abstract Reference treatment of advanced prostate cancer (PCa) relies on pharmacological or surgical androgen deprivation therapy. However, it is only temporarily efficient as tumor cells inevitably adapt to the low testosterone environment and become hormone-refractory (HRPCa). We observed that androgen removal in HRPCa-derived LNCaP cells causes different alterations in their Ca(2+) homeostasis among which a reduction of ER Ca(2+) content. We show that the decrease in [Ca(2+)]ER is due to a modest overexpression of type 1 IP3R and a threefold increased phosphorylation of IP3R1 on Ser-1716, a protein kinase A (PK...
Source: Cell Calcium - February 18, 2015 Category: Cytology Authors: Boutin B, Tajeddine N, Monaco G, Molgo J, Vertommen D, Rider M, Parys JB, Bultynck G, Gailly P Tags: Cell Calcium Source Type: research

Glucose-regulated protein 78 mediates the anticancer efficacy of shikonin in hormone-refractory prostate cancer cells
Abstract Glucose-regulated protein 78 (GRP78) is a key modulator of prostate cancer progression and therapeutic resistance. Prostate cancer is a worldwide health problem, and therapeutic resistance is a critical obstacle for the treatment of hormone-refractory prostate cancer patients. Shikonin inhibits prostate cancer proliferation and metastasis. However, the role of GRP78 in the cytotoxic effect of shikonin in prostate cancer cells remains unclear. GRP78 expression was abolished using small interfering RNA (siRNA), and the anticancer effects of shikonin were assessed using MTT assays, the XCELLigence biosensor,...
Source: Tumor Biology - February 10, 2015 Category: Cancer & Oncology Source Type: research

A novel hydroxysuberamide derivative potentiates MG132‐mediated anticancer activity against human hormone refractory prostate cancers—the role of histone deacetylase and endoplasmic reticulum stress
CONCLUSIONSThe data suggest that WJ25591 inhibited HDAC activity, leading to cell‐cycle arrest and inhibition of DNA repair. Caspase cascades are subsequently triggered to execute cell apoptosis. MG‐132 dramatically sensitizes WJ25591‐mediated apoptosis, at least partly, through ER stress response. The data also reveal that combination of HDAC inhibitors and proteasome inhibitors may be a potential strategy against hormone‐refractory prostate cancers. Prostate © 2013 Wiley Periodicals, Inc.
Source: The Prostate - June 28, 2013 Category: Urology & Nephrology Authors: Yi‐Cheng Chen, Wei‐Jan Huang, Jui‐Ling Hsu, Chia‐Chun Yu, Wei‐Ting Wang, Jih‐Hwa Guh Tags: Original Article Source Type: research

PSA-responsive and PSMA-mediated multifunctional liposomes for targeted therapy of prostate cancer.
In this study, we constructed a dual-modified liposome that incorporated PSA-responsive and PSMA-mediated liposomes and potentially offers double selectivity for PC. The folate moiety binds quickly to PSMA-positive tumors, and the PSA-responsive moiety is cleaved by PSA that was enriched in tumor tissues. The activated liposomes (folate and cell-penetrating peptides dual-modifications) are subsequently taken up by the tumor cells via polyarginine's penetrating effects and receptor-mediated endocytosis. To corroborate these assumptions, a series of experiments were conducted, including PSA-responsive peptide hydrolysis kine...
Source: Biomaterials - June 15, 2013 Category: Materials Science Authors: Xiang B, Dong DW, Shi NQ, Gao W, Yang ZZ, Cui Y, Cao DY, Qi XR Tags: Biomaterials Source Type: research