In western nations, a typical gynecological cancer is endometrial cancer. Tumor metastasis and invasion are correlated with the expiries and prognosis of most patients suffering from cancer. Epithelial to mesenchymal transition (EMT) is a vital process in cancer metastasis. The transforming growth factor-beta (TGF-β) signaling pathway prompts EMT and aids the capacity of cancer cells’ migration and invasion. A flavonoid isolated from licorice and bean sprouts is known as Isoliquiritigenin (ISL), which exhibits antitumor activities. Yet, it is uncertain if the ISL has any effects on endometrial cancer’s EMT and TGF-β signaling pathway. Subsequently, the objective of the research was to explore the antimetastatic capability of ISL on endometrial cancer.
The researchers performed two studies – in vivo and in vitro. In the former study, nude mice were implanted with Hec-1A. For one month, ISL was administered to them using i.p. injections. In the latter, ISL was used to medicate human endometrial cell lines (HEC-1A, RL95-2, and Ishikawa). Afterward, they were put through immunoblotting analysis, Immunofluorescence analysis, and migration assay.
The former study showed that peritoneal dissemination was decreased by ISL. In addition, there was a reduction in the amount of TGFβRI, p-Smad2, N-cadherin, and MMP-9 expression. Other than that, E-cadherin expression levels were greater than before. Meanwhile, the latter study demonstrated that ISL decreased the expression of N-cadherin. But, it also boosted the expression of E-cadherin. In addition, ISL repressed the cancer cell’s migration and invasion using the TGF-β/Smad signaling pathway. The research is one of the first to investigate ISL’s anti-metastasis effects on endometrial cancer in both in vivo and in vitro studies. ISL successfully repressed cancer cells’ migration and invasion with the help of the TGF-β/Smad signaling pathway. Therefore, ISL has demonstrated its capabilities in endometrial cancer’s therapeutic treatment.
Link:www.esmoopen.com/article/S2059-7029(20)31815-9/fulltext#relatedArticles
