权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Chemoprevention of Prostate Cancer by Curcumin

姜黄素化学预防前列腺癌

基本信息

批准号：
7322102
负责人：
Sharmila Shankar
金额：
$ 6.88万
依托单位：
UNIVERSITY OF TEXAS HLTH CTR AT TYLER
依托单位国家：
美国
项目类别：
财政年份：
2007
资助国家：
美国
起止时间：
2007-07-10 至 2009-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7322102
关键词：
Androgen Receptor Androgens Animal Model Anti-Inflammatory Agents Anti-inflammatory Antioxidants Apoptosis Apoptotic Biological Response Modifier Therapy Cancer Etiology Caspase Cells Cessation of life Chemoprevention Chemopreventive Agent Clinical Trials Cultured Cells Curcumin Data Development Disease Employee Strikes Epidemiologic Studies Event Exhibits Family Food Generations Goals Growth Hormones Implant In Vitro Induction of Apoptosis Knowledge LNCaP Malignant neoplasm of prostate Mitochondria Modeling Molecular Mus North America Nude Mice Operative Surgical Procedures PC3 cell line Pathway interactions Pigments Prevention strategy Prostate Prostatic Neoplasms Radiation therapy Reactive Oxygen Species Refractory Research Design Resistance Role Staging TNFSF10 gene TP53 gene Testing Tumeric Tumor Tissue Up-Regulation base cancer cell cancer diagnosis caspase-3 caspase-8 chemotherapy dietary constituent hormone therapy in vivo interest member men neoplastic cell novel novel strategies prostate cancer prevention receptor response tumor tumor initiation

项目摘要

DESCRIPTION (provided by applicant): Curcumin, a pigment in turmeric, possesses anti-inflammatory, antioxidant, antitumor, neuroprotective, and immunomodulatory activities. It exerts striking inhibitory effects on diverse cellular events associated with tumor initiation, promotion, and progression, thus holds great promise for development as a chemopreventive agent for prostate cancer. The rationale for using curcumin as a chemopreventive agent comes from the epidemiological studies and our preliminary data. Curcumin induces apoptosis through engagement of both mitochondrial and death receptor pathways of apoptosis. Furthermore, curcumin, although effective alone, can sensitize prostate cancer cells to TRAIL. However, the mechanisms by which curcumin induces sensitivity in prostate cancer cells are not known. Studies proposed in this application will not only fill this gap in our knowledge but also generate data that will guide us in formulating curcumin and TRAIL-based strategies for prevention and/or treatment of human prostate cancers. Based on our preliminary findings, we hypothesize that curcumin will be highly effective in suppressing growth of human prostate cancer cells due to its ability to induce apoptosis through upregulation of death receptors and proapoptotic members of Bcl-2 family and activation of caspase(s). We propose to test this hypothesis by: (1) Determining the molecular mechanisms by which curcumin inhibits proliferation and induces apoptosis in human prostate cancer cells, and (2) Determining the effects of curcumin and/or TRAIL on growth of human prostate cancer cells orthotopically implanted in nude mice. In Specific Aim 2, tumors from the vehicle treated control and curcumin and/or TRAIL treated mice will be examined to determine the extent to which curcumin and/or TRAIL-induced molecular changes pertaining to apoptosis induction observed in cultured cells (Specific Aim 1) correlate with their effects in vivo. Specifically, studies are designed to determine the contribution of mitochondrial and/or death receptor pathways in curcumin-induced apoptosis. In summary, the studies proposed in this application will define the mechanism by which curcumin inhibits growth of human prostate cancer cells and determine in vivo efficacy of curcumin and/or TRAIL against prostate cancer using an animal model, which is a prerequisite for initiation of clinical trials to determine its activity against human prostate cancer. We expect the proposed studies to yield data in support of our hypothesis and to serve as a critical step in developing new approaches to prostate cancer prevention.

描述（由申请人提供）：