ANTICANCER MECHANISMS OF LYCOPENE ACTION

番茄红素的抗癌机制

• 批准号: 7381573
• 负责人: LOYD H BURGESS
• 金额: $ 18.86万
• 依托单位: UNIVERSITY OF NORTH DAKOTA
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-05-01 至 2007-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7381573
• 关键词: ANTICANCER; MECHANISMS; LYCOPENE; ACTION

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. Introduction: Our goal is to determine whether some of the anticarcinogenic properties of lycopene are mediated through the stimulation gap junctional communication. This year we are investigating whether lycopene reduces cell proliferation and if so, whether production of gap junctional connexin proteins and mRNAs are affected in a dose-dependent fashion. Methods: We screened six human cell lines to date: Hs-578Bst, noncancerous breast; Hs-578T, breast carcinoma; Hs-68, noncancerous skin fibroblast; DU-145, prostate carcinoma; ZR-75-1, breast carcinoma; A549, lung carcinoma; and IMR-90, noncancerous lung. Cells were exposed to a dose-range of lycopene from 10-10 M to 10-5 M for 1-3 days and then counted electronically. The cells were grown to confluency, then treated with lycopene, then had their RNA separated, converted to cDNA and tested by PCR for expression of the connexin 43 gene. Results: The ZR-75-1 cells were not usable, the Hst-578T, Hst-578Bst and IMR-90 are still being screened. The DU-145 and Hs-68 cells have shown no significant changes to cell proliferation due to lycopene. They express the connexin 43 mRNAs across the dose-range. Discussion: Studies are still incomplete on these aims and building construction has delayed progress. The results show that several cell lines are not affected by lycopene because their proliferation and expression of the connexin 43 and therefore will be usable for further studies. This adds evidence to our hypothesis that the anticarcinogenic effect of lycopene is its effect on the gap junctional communication not cell proliferation. The project will continue with these studies for the remainder of the current budget period and into the next. We will add Real-time PCR to quantify the mRNA expression and use ELISA and western blotting to examine connexin protein expression. Additional cell lines will be added as planned. We will move to a new lab and building this budget period.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。简介：我们的目标是确定番茄红素的抗癌特性是否通过刺激缝隙连接通讯介导。今年我们正在研究番茄红素是否会减少细胞增殖，如果是的话，间隙连接蛋白和mRNA的产生是否会以剂量依赖的方式受到影响。 研究方法：迄今为止，我们筛选了六种人类细胞系：Hs-578 Bst，非癌性乳腺; Hs-578 T，乳腺癌; Hs-68，非癌性皮肤成纤维细胞; DU-145，前列腺癌; ZR-75-1，乳腺癌; A549，肺癌;和IMR-90，非癌性肺。 将细胞暴露于10-10 M至10-5 M剂量范围的番茄红素1-3天，然后电子计数。细胞生长至汇合，然后用番茄红素处理，然后分离它们的RNA，转化为cDNA，并通过PCR检测连接蛋白43基因的表达。 结果：ZR-75-1细胞不能使用，Hst-578 T、Hst-578 Bst和IMR-90仍在筛选中。DU-145和Hs-68细胞没有显示出由于番茄红素引起的细胞增殖的显著变化。它们在剂量范围内表达连接蛋白43 mRNA。 讨论：关于这些目标的研究仍然不完整，建筑工程拖延了进展。结果表明，几种细胞系不受番茄红素的影响，因为它们的增殖和连接蛋白43的表达，因此将可用于进一步的研究。 这为我们的假设增加了证据，即番茄红素的抗癌作用是它对差距连接通讯的作用，而不是细胞增殖。 本项目将在本预算期剩余时间和下一个预算期继续进行这些研究。我们将增加Real-time PCR来定量mRNA的表达，并使用ELISA和western blotting来检测连接蛋白的表达。将按计划添加其他细胞系。我们将搬到一个新的实验室，并在这个预算期内建造。