RESUMO
Ensemble clustering integrates a set of base clustering results to generate a stronger one. Existing methods usually rely on a co-association (CA) matrix that measures how many times two samples are grouped into the same cluster according to the base clusterings to achieve ensemble clustering. However, when the constructed CA matrix is of low quality, the performance will degrade. In this article, we propose a simple, yet effective CA matrix self-enhancement framework that can improve the CA matrix to achieve better clustering performance. Specifically, we first extract the high-confidence (HC) information from the base clusterings to form a sparse HC matrix. By propagating the highly reliable information of the HC matrix to the CA matrix and complementing the HC matrix according to the CA matrix simultaneously, the proposed method generates an enhanced CA matrix for better clustering. Technically, the proposed model is formulated as a symmetric constrained convex optimization problem, which is efficiently solved by an alternating iterative algorithm with convergence and global optimum theoretically guaranteed. Extensive experimental comparisons with 12 state-of-the-art methods on ten benchmark datasets substantiate the effectiveness, flexibility, and efficiency of the proposed model in ensemble clustering. The codes and datasets can be downloaded at https://github.com/Siritao/EC-CMS.
RESUMO
Background: Taraxasterol (TX), a pentacyclic triterpene, is one of the main active constituents isolated from Taraxacum officinale. A growing number of studies have reported that TX exhibits a wide range of biological activities such as anti-oxidative, anti-inflammatory, and neuro-protective effects. Recently, TX has been demonstrated to be a potential drug candidate for treatment of some types of cancers. However, the specific role of TX in melanoma remains unclear.Purpose: In this study, we aimed at exploration of the effect of TX on melanoma cell viability, apoptosis, migration, invasion, and epithelial-mesenchymal transition (EMT) as well as the underlying mechanisms.Research design: A375 and SK-MEL-28 cells were treated with various concentrations of TX for different times. Cell viability was measured using CCK-8 assay. Cell apoptosis was determined by flow cytometry. Transwell assays were performed to measure cell migration and invasion. The expression of E-cadherin, α-catenin, N-cadherin, vimentin, p-PI3K, PI3K, p-Akt and Akt was detected using western blot.Results: The study showed that TX induced A375 and SK-MEL-28 cell apoptosis. Furthermore, exposure to TX inhibited A375 and SK-MEL-28 cell migration and invasion. Besides, the EMT process was reversed in A375 and SK-MEL-28 cells after TX treatment. We also observed that TX reduced the protein expression of p-PI3K and p-Akt; thus, inhibiting activity of the PI3K/Akt pathway in A375 and SK-MEL-28 cells. In addition, TX treatment increased the levels of reactive oxygen species (ROS) in A375 and SK-MEL-28 cells, and treatment with the ROS scavenger NAC significantly rescued TX-induced down-regulation of p-PI3K and p-Akt in A375 and SK-MEL-28 cells.Conclusions: In conclusion, our study demonstrated that TX induced ROS accumulation followed by inactivation of the PI3K/Akt pathway and subsequently attenuated melanoma progression, suggesting that TX may be a potential candidate for treatment of melanoma.
