人工合成型丹蔘化合物對人類前列腺癌細胞生長及轉移的影響;Effects of the synthetic Danshen compounds on human prostate cancer cells growth and metastasis

NCUIR > college of Health Sciences and Technology > Graduate Institute of Life Science > Electronic Thesis & Dissertation > Item 987654321/89270

Please use this identifier to cite or link to this item: http://ir.lib.ncu.edu.tw/handle/987654321/89270

Title:	人工合成型丹蔘化合物對人類前列腺癌細胞生長及轉移的影響;Effects of the synthetic Danshen compounds on human prostate cancer cells growth and metastasis
Authors:	陳詣淇;Chen, Yi-Qi
Contributors:	生命科學系
Keywords:	前列腺癌;人工合成型丹蔘化合物;生長;轉移;Prostate cancer;Synthetic Danshen compounds;Growth;Metastasis
Date:	2022-09-29
Issue Date:	2022-10-04 11:03:59 (UTC+8)
Publisher:	國立中央大學
Abstract:	前列腺癌 (PCa) 是男性第二常見的癌症，佔男性癌症診斷的 15% 和所有癌症病例的 8%。丹蔘（Salvia miltiorrhiza Bunge）在中藥中被廣泛用於治療冠狀動脈疾病和腦血管疾病，且副作用較小，並被發現可抑制前列腺癌的細胞生長、遷移和侵襲。在本研究中我們選擇了三種合成丹蔘化合物，為化合物 4、5、6，其化學結構與天然丹蔘化合物相似。我們假設化合物 4、5、6 可能對前列腺癌具有抗癌活性。首先我們觀察到化合物 4、5、6 以劑量和時間依賴性方式降低雄激素依賴性 (LNCaP-FGC) 和雄激素非依賴性 (PC-3, DU145) 人類前列腺癌細胞的細胞數及細胞存活率。此外利用 BrdU 細胞增殖測定以及細胞週期分析發現到化合物4、5、6 可以影響前列腺癌 DNA 合成能力和 G1 phase，然而這些數據表明化合物 4、5、6 對前列腺癌細胞的生長增殖具有抑制作用。當檢測信號蛋白時，我們發現化合物 4、5、6 在 LNCaP-FGC 和 PC-3 細胞中抑制 AKT 的磷酸化，這些數據表明化合物 4、5、6 可能通過 AKT 途徑抑制前列腺癌細胞的生長。此外，我們發現化合物 4、5、6 抑制了 LNCaP-FGC 細胞中雄激素受體 (AR) 蛋白的表達，並且該化合物顯著抑制了 PC-3、DU-145 細胞的轉移及侵入。總之，化合物 4、5、6 通過 AR 和 AKT 途徑抑制雄激素依賴性前列腺癌細胞的生長，以及通過 AKT 或細胞週期蛋白途徑抑制雄激素非依賴性前列腺癌細胞的生長。;Prostate cancer (PCa) is the second most commonly diagnosed cancer in men, representing 15% of male cancer diagnosis and 8% of all cancer cases. Danshen (Salvia miltiorrhiza Bunge) has been widely used in traditional Chinese medicine for the treatment of coronary artery disease and cerebrovascular diseases with minimal side effects, and it has been found to inhibit cell growth, migration and invasion in prostate cancer. Recently, we selected a synthetic compound named compound 4, 5, 6, which has a chemical structure similar to native Danshen compounds. We hypothesized that compound 4, 5, 6, may have anti-cancer activity against prostate cancer. First, we observed that compound 4, 5, 6 reduced the cell number and cell viability in androgen-dependent (LNCaP-FGC) and androgen-independent (PC-3, DU145) human prostate cancer cells in in high doses and low doses over time. In addition, using BrdU cell proliferation assay and cell cycle analysis, it was found that compounds 4, 5, and 6 can affect the DNA synthesis capacity and G1 phase of prostate cancer cells. When signaling proteins were examined, we found that compound 4, 5, 6 suppressed phosphorylation of AKT in both LNCaP-FGC and PC-3 cells. These data suggest that compound 4, 5, 6 may inhibit prostate cancer cell growth through the AKT pathway. Moreover, we discovered that compound 4, 5, 6 suppressed the expression of androgen receptor (AR) protein in LNCaP-FGC cells and that the compound significantly suppressed the migration of PC-3 cells. In conclusions, compound 4, 5, 6 suppressed growth of androgen-dependent prostate cancer cells through the AR and AKT pathways, as well as inhibiting growth of androgen-independent prostate cancer cells through the AKT or cell cycle protein pathway.
Appears in Collections:	[Graduate Institute of Life Science] Electronic Thesis & Dissertation

Files in This Item:

File	Description	Size	Format
index.html		0Kb	HTML	93	View/Open

社群 sharing

Loading...