ANTICANCER MECHANISMS OF LYCOPENE ACTION

番茄红素的抗癌机制

• 批准号: 7610172
• 负责人: LOYD H BURGESS
• 金额: $ 17.76万
• 依托单位: UNIVERSITY OF NORTH DAKOTA
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-05-01 至 2008-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7610172
• 关键词: Affect; Binding; Cancer cell line; Cell Communication; Cell Proliferation; Cells; Chemopreventive Agent; Communication; Computer Retrieval of Information on Scientific Projects Database; Connexins; Dose; Epidemiologic Studies; Funding; Gap Junctions; Goals; Grant; Health Benefit; Institution; Ligands; Malignant Neoplasms; Messenger RNA; Non-Malignant; Normal Cell; Property; Research; Research Personnel; Resources; Safety; Source; United States National Institutes of Health; cancer cell; cancer risk; computational chemistry; dietary supplements; lycopene; neoplastic cell; protein expression; receptor

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The long-term goal of this study is to investigate the anticarcinogenic properties of lycopene at the cellular level. Our first hypothesis is that one of lycopenes anticarcinogenic properties is due to its ability to suppress the proliferation of cancer cells. Our second hypothesis is that one of lycopenes anticarcinogenic properties is due to its ability to increase or renew gap junctional connexin (Cx) protein expression. Therefore, lycopene maintains or creates gap junctional communication from cell to cell, which can control proliferation of neoplastic cells from surrounding normal cells. Our third hypothesis is that there are additional receptors and ligands in cells that can bind lycopene, which may be determined with computational chemistry. Specific Aim 1 for the first hypothesis: we will determine if the anticarcinogenic properties of lycopene include the ability to reduce cell proliferation in the cancer cell lines. Specific Aim 2 for the second hypothesis: we will determine if lycopene, in a dose-dependent fashion, affects the mRNA and protein expression of gap junctional connexins and gap junctional communication (GJC) in cultured cancer cells and nonmalignant cells. We will determine if lycopene treatment is restoring the gap junction function and expression in cancer cells compare the function in nonmalignant cells. Specific Aim 3 for the third hypothesis: we will investigate the potential binding of lycopene to cancer-related targets by using computational chemistry. This will help to determine what receptors may be binding to the lycopene. Epidemiological studies have shown that lycopene is associated with a reduced risk of cancer. Lycopene has been promoted and sold as a dietary supplement with claims about its anticancer and other health benefits. The efficacy and safety of lycopene has not been specifically evaluated nor has the mechanism of lycopene action been determined.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 本研究的长期目标是在细胞水平上研究番茄红素的抗癌特性。 我们的第一个假设是番茄红素的抗癌特性是由于它能够抑制癌细胞的增殖。 我们的第二个假设是番茄红素其抗癌特性是由于其能够增加或更新间隙连接蛋白（Cx）蛋白表达。 因此，番茄红素维持或产生细胞与细胞之间的间隙连接通讯，这可以控制肿瘤细胞从周围正常细胞增殖。 我们的第三个假设是，细胞中有额外的受体和配体可以结合番茄红素，这可以用计算化学来确定。 第一个假设的具体目标1：我们将确定番茄红素的抗癌特性是否包括减少癌细胞系中细胞增殖的能力。 第二个假设的具体目标2：我们将确定番茄红素是否以剂量依赖性方式影响培养的癌细胞和非恶性细胞中间隙连接蛋白和间隙连接通讯（GJC）的mRNA和蛋白表达。 我们将确定番茄红素治疗是否恢复癌细胞中的差距连接功能和表达，并与非恶性细胞中的功能进行比较。 第三个假设的具体目标3：我们将通过使用计算化学研究番茄红素与癌症相关靶点的潜在结合。 这将有助于确定哪些受体可能与番茄红素结合。 流行病学研究表明，番茄红素与降低癌症风险有关。 番茄红素已被推广和销售作为膳食补充剂，声称其抗癌和其他健康益处。 番茄红素的有效性和安全性还没有被专门评估，也没有番茄红素作用的机制被确定。