癌症發病率在全球範圍內迅速增長，包括台灣在內，肺癌成為一個突出的問題。由於癌細胞的侵襲性，患者常常在被檢測和治療之前就達到了3期。近年來，東方醫學作為一種經濟高效、綜合全面的治療方法受到了廣泛關注。該研究使用了BP010W在100 μg/ml濃度下的數據，通過36小時的實驗組展示了其出色的抑制肺癌細胞遷移的能力。使用DAVID程序對包含1375個基因的進一步分析表明可能參與了雌激素信號通路，為未來的研究提供了前景，並驗證了研究結果。發現了三條獨立的遷移途徑，並且結果顯示與雌激素信號系統相關的基因明顯下調，特別是MMP13、ZEB1、SNAI1、VIM、CDH2和ICAM1。此外，使用連接圖譜（cMap）對33個上調基因和150個下調基因進行比較，展示了Erteberel及其與雌激素信號通路的關係。該研究進一步證實了BP010W通過調節雌激素信號系統來減少肺癌細胞遷移的能力。 BP010W中被確認的組分之一，Solasodine，顯示出對肺癌細胞具有強效的抑製作用。包括細胞阻塞試驗和存活性評估在內的實驗顯示了雌激素的促遷移效應以及Solasodine在限制遷移中的關鍵作用。;Cancer incidence is quickly growing globally, including in Taiwan, with lung cancer being a prominent concern. Because of the aggressive nature of cancer cell migration, patients frequently reach stage 3 before being detected and treated. Oriental medicine has received a lot of attention in recent years as a cost-effective and comprehensive approach to treatment. The study uses data from BP010W at a concentration of 100 μg/ml in a 36-hour group to demonstrate its extraordinary ability to block lung cancer cell migration. Further analysis encompassing 1375 genes using the DAVID program suggests a likely participation of the estrogen pathway, giving prospects for future research and validating the study′s findings. Three separate migratory routes are discovered, and the results show a considerable downregulation of genes linked with the estrogen signalling system, notably MMP13, ZEB1, SNAI1, VIM, CDH2 and ICAM1. Furthermore, using the Connectivity Map (cMap) to compare 33 up-regulated genes and 150 down-regulated genes demonstrates erteberel and its relationship with the estrogen signalling pathway. This study adds to the evidence that BP010W has the ability to reduce lung cancer cell migration via modulating the estrogen signalling system. Solasodine, one of the recognized components of BP010W, appears as a significant element with potent inhibitory effects on lung cancer cells. Experiments, including cell-blocking tests and viability evaluations, show estrogen′s pro-migratory effect and the critical role of Solasodine in limiting migration.
