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3. Dihydrotanshinone-I modulates Epithelial Mesenchymal Transition (EMT) Thereby Impairing Migration and Clonogenicity of Triple Negative Breast Cancer Cells

Author

Akanksha Kashyap, Sheikh Mohammad Umar, Chandra Prakash Prasad, and Arundhathi Dev J R

Subjects
Epithelial-Mesenchymal Transition, cell migration, epithelial mesenchymal transition, Vimentin, Triple Negative Breast Neoplasms, Salvia miltiorrhiza, Cell Movement, Cell Line, Tumor, Biomarkers, Tumor, Humans, MTT assay, Epithelial–mesenchymal transition, Clonogenic assay, Furans, Cell Proliferation, biology, Chemistry, Plant Extracts, Mesenchymal stem cell, CD44, Quinones, dihydrotanshinone-I, Cell migration, General Medicine, Phenanthrenes, biology.protein, Cancer research, TNBC, Research Article
Abstract

Background Salvia miltiorrhiza Bunge (Danshen), has been used for its therapeutic value in Traditional Chinese Medicine (TCM), for almost a thousand years. Dihydrotanshinone-I (DHTS) is a lipophilic compound isolated from the plant Salvia miltiorrhiza that has been shown to induce anti-proliferative and apoptotic effects on breast cancer cells. In the present study, we investigated the anti-migratory effect of DHTS on TNBC cell lines by studying the Epithelial Mesenchymal Transition (EMT) changes. Methods IC50 values for DHTS in TNBC breast cancer cells were either discovered by literature search or by performing MTT assay. DHTS effect on EMT markers (viz. CD44, E-cadherin, Vimentin, N-cadherin, and active β-catenin) was studied using western blotting. Association between EMT and migration was further carried out in DHTS treated TNBC cells by wound healing assay. Cancer stemness and proliferation potential were further accessed using colony formation assay. Results MTT assay revealed IC50 of MDA-MB-468 cells at 2 µM for 24 h. Subsequently, DHTS treatment in TNBC cell lines (MDA-MB-468 and MDA-MB-231) led to decrease in mesenchymal markers i.e. vimentin, N-cadherin and, active β-catenin. DHTS treated MDA-MB-468 cells showed a decrease in adhesion protein CD44 and an increase in epithelial protein E-cadherin. Additionally, a decrease in EMT potential was positively associated with the inhibition of migration and clonogenic potential in DHTS treated TNBC cells. Conclusion In this study, we have demonstrated for the first time that DHTS has the potential to inhibit the migration and clonogenicity of highly aggressive TNBC cells by obstructing Epithelial to Mesenchymal Transition.

Published
2021

6. Quercetin Impairs HuR-Driven Progression and Migration of Triple Negative Breast Cancer (TNBC) Cells.

Author

Umar, Sheikh Mohammad, Patra, Sushmita, Kashyap, Akanksha, Dev J R, Arundhathi, Kumar, Lalit, and Prasad, Chandra Prakash

Subjects
DISEASE progression, RNA-binding proteins, CYTOSKELETAL proteins, ANTINEOPLASTIC agents, RNA, CELL receptors, CANCER relapse, QUERCETIN, CELL motility, GENE expression, CELL adhesion molecules, CELL lines, BREAST tumors
Abstract

In the present study, we have explored the prognostic value of HuR gene as well as protein in breast cancers. Furthermore, we have also investigated the HuR therapeutic relevance in TNBCs, which is an aggressive breast cancer subtype. Using an online meta-analysis tool, we found that HuR protein overexpression positively correlates with reduced overall survival of TNBC patients (p = 0.028). Furthermore, we demonstrated that the TNBC breast cancer cell lines i.e., MDA-MB-231 and MDA-MB-468 are good model systems to study HuR protein, as they both exhibit a significant amount of cytoplasmic HuR (active form). Quercetin treatment significantly inhibited the cytoplasmic HuR in both TNBC cell lines. By using specific HuR siRNA, we established that quercetin-mediated inhibition of adhesion and migration of TNBC cells is dependent on HuR. Upon analyzing adhesion proteins i.e., β-catenin and CD44, we found that quercetin mediated effect on TNBC adhesion and migration was through the HuR-β-catenin axis and CD44, independently. Overall, the present results demonstrate that elevated HuR levels are associated with TNBC progression and relapse, and the ability of quercetin to inhibit cytoplasmic HuR protein provides a rationale for using it as an anticancer agent for the treatment of aggressive TNBCs. Supplemental data for this article is available online at at 10.1080/01635581.2021.1952628. [ABSTRACT FROM AUTHOR]

Published
2022
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