scholarly journals MiR-1976 knockdown promotes epithelial–mesenchymal transition and cancer stem cell properties inducing triple-negative breast cancer metastasis

2020 ◽  
Vol 11 (7) ◽  
Author(s):  
Jingyi Wang ◽  
Minghui Li ◽  
Xu Han ◽  
Hui Wang ◽  
Xinyang Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Triple Negative Breast Cancer ◽  
Cancer Metastasis ◽  
Triple Negative ◽  
Epithelial Mesenchymal Transition ◽  
Breast Cancer Metastasis ◽  
Mesenchymal Transition

scholarly journals Cooperation of Cancer Stem Cell Properties and Epithelial-Mesenchymal Transition in the Establishment of Breast Cancer Metastasis

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Tetsu Hayashida ◽  
Hiromitsu Jinno ◽  
Yuko Kitagawa ◽  
Masaki Kitajima
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Cancer Progression ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Metastatic Tumor ◽  
Breast Cancer Metastasis ◽  
Cell Junctions ◽  
Mesenchymal Transition

Epithelial-mesenchymal transition (EMT) is a multistep process in which cells acquire molecular alterations such as loss of cell-cell junctions and restructuring of the cytoskeleton. There is an increasing understanding that this process may promote breast cancer progression through promotion of invasive and metastatic tumor growth. Recent observations imply that there may be a cross-talk between EMT and cancer stem cell properties, leading to enhanced tumorigenicity and the capacity to generate heterogeneous tumor cell populations. Here, we review the experimental and clinical evidence for the involvement of EMT in cancer stem cell theory, focusing on the common characteristics of this phenomenon.

scholarly journals The role of EMT-related lncRNA in the process of triple-negative breast cancer metastasis

2021 ◽  
Vol 41 (2) ◽  
Author(s):  
Haomeng Zhang ◽  
Jiao Wang ◽  
Yulong Yin ◽  
Qingjie Meng ◽  
Yonggang Lyu
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Cancer Metastasis ◽  
Triple Negative ◽  
Epithelial Mesenchymal Transition ◽  
Breast Cancer Metastasis ◽  
Signal Pathways ◽  
Mesenchymal Transition ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Triple-negative breast cancer (TNBC) is the most malignant and fatal subtype of breast cancer, which has characterized by negativity expression of ER, PR, and HER2. Metastasis is the main factor affecting the prognosis of TNBC, and the process of metastasis is related to abnormal activation of epithelial–mesenchymal transition (EMT). Recent studies have shown that long non-coding RNA (LncRNA) plays an important role in regulating the metastasis and invasion of TNBC. Therefore, based on the metastasis-related EMT signaling pathway, great efforts have confirmed that LncRNA is involved in the molecular mechanism of TNBC metastasis, which will provide new strategies to improve the treatment and prognosis of TNBC. In this review, we summarized many signal pathways related to EMT involved in the transfer process. The advances from the most recent studies of lncRNAs in the EMT-related signal pathways of TNBC metastasis. We also discussed the clinical research, application, and challenges of LncRNA in TNBC.

scholarly journals Effect of tetrandrine combined with arsenic trioxide on stem cells of triple negative breast cancer

2019 ◽  
Author(s):  
Yubo Guo ◽  
Yingyi Fan ◽  
Ruixian Wu ◽  
Xiaohua Pei
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Flow Cytometry ◽  
Stem Cell ◽  
Arsenic Trioxide ◽  
Triple Negative Breast Cancer ◽  
Cancer Metastasis ◽  
Triple Negative ◽  
Breast Cancer Metastasis ◽  
Blue Staining

Abstract Background Although the triple negative breast cancer is sensitive to chemotherapy, breast cancer stem cells (BCSCs) is the origin of tumor chemotherapy resistance, tumor recurrence and tumor invasion and metastasis. This study aims to examine the effect of tetrandrine combine with arsenic trioxide on BCSCs and potential mechanism of anti- triple negative breast cancer metastasis. Methods We cultured the triple negative breast cancer cell MDA-MB-231 and induced BCSCs sphere formation by serum-free medium for 5 days. In the MDA-MB-231 cell and MDA-MB-231 stem cell, we compared the ratio of CD44+/CD24- and sorted stem cells by flow cytometry, the expression of Oct4 and Sox2mRNA were by rt-PCR, invasion ability were by Transwell assay. We subsequently measured the effect of tetrandrine combine with arsenic trioxide on BCSCs proliferation by CCK8 method. The stem cell morphology observation was by trypan blue staining. Stem cell cycle and apoptosis were evaluated by flow cytometry. Western Blot was used to measure the protein levels of Hedgehog, Notch1 and PTEN signaling of BCSCs. Results The ratio of CD44+/CD24- in MDA-MB-231 stem cells was 95.0%, while MDA-MB-231 cell was 89.3%. The invasion number of MDA-MB-231 stem cell was significantly higher than that of MDA-MB-231 cells (p<0.01). Furthermore, we demonstrated that tetrandrine and arsenic trioxide could inhibit the BCSCs proliferation. Tetrandrine combine with arsenic trioxide could significantly promote the apoptosis (p<0.01) and increase the percentage of G0/G1 phase and decrease the G2/M phase (p<0.01) of BCSCs. Compared with the control group, arsenic trioxide, tetrandrine and the combined group could significantly reduce the expression of GLI1 and SMO and increase the expression of PTEN protein (P<0.05). Conclusions These findings revealed that tetrandrine combined with arsenic trioxide could suppress the proliferation and induce apoptosis of BCSCs by decreased Gli and SMO expression and increased PTEN expression. Targeting BCSCs treatment, this study provides potential therapeutic drugs against triple negative breast cancer metastasis.

scholarly journals Potential targeted therapy: The role of MicroRNAs in breast cancer metastasis via epithelial-mesenchymal transition and cancer stem cell regulation

2021 ◽  
Vol 2 (1) ◽  
Author(s):  
Pamungkas Bagus Satriyo
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Targeted Therapy ◽  
Cancer Stem Cell ◽  
Cancer Treatment ◽  
Cancer Metastasis ◽  
Metastatic Breast ◽  
Breast Cancer Metastasis ◽  
Mesenchymal Transition ◽  
Junction Protein

Abstract In the advancement of breast cancer treatment, metastatic breast cancer is remaining as an incurable disease. It contributes to almost 90% of cancer-related death in breast cancer cases. Epithelial to Mesenchymal Transition (EMT) is a serial change of the epithelial cell to gain the mesenchymal-like phenotype. In cancer, the cells that undergo the EMT lose the adherent junction protein, cell polarity, and gain the invasive phenotype. Recent studies showed that the EMT induces the cancer stem cell-like phenotypes in cancer cells. These cells possess self-renewal ability, and multi-lineage differentiation capacity to generate the new bulk of tumor during cancer distant metastasis. Both EMT and cancer stem cells take responsibility in drug-resistant, and relapse cases in breast cancer. In the last decades, a new type of non-coding RNA, microRNA (miR) shows have an important role in the normal physiological and pathophysiological condition such as cancer. Recent studies revealed that the EMT is regulated by microRNAs. In this review, we discussed the microRNAs regulation on the EMT process through TGF-β, and Wnt signaling pathways in breast cancer. Understanding of microRNA regulation in EMT in breast cancer metastasis gives a chance to explore a new therapy approach to improve the prognosis of breast cancer patients. In addition, we also explored several potential approaches targeting microRNA as a new approach of cancer treatment.   Keywords: breast cancer, microRNA, EMT, metastasis, targeted therapy.

scholarly journals Huaier polysaccharides suppress triple-negative breast cancer metastasis and epithelial-mesenchymal transition by inducing autophagic degradation of Snail

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yuan Tian ◽  
Jin Wu ◽  
Lingjuan Zeng ◽  
Linxi Zhou ◽  
Ying Hu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Cell Invasion ◽  
Cancer Metastasis ◽  
Triple Negative ◽  
Epithelial Mesenchymal Transition ◽  
Inhibitory Effects ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration

Abstract Background Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, and the targeted therapies are lacking for this type of cancer. We previously demonstrated that Huaier effectively improve 5-year OS and DFS in stage III TNBC patients, and the polysaccharides of Huaier (PS-T) have been identified as the major components of Huaier. However, the mechanisms of anti-tumor action of PS-T is unclear. This study aimed to investigate the effect of PS-T on TNBC cell invasion and migration. Results This study showed that PS-T inhibited cell invasion and migration both in vitro and in vivo by inducing autophagy to suppress epithelial-mesenchymal transition (EMT). Autophagy inhibitor LY294002 or knockdown of ATG5 suppressed the inhibitory effects of PS-T. In addition, as a key transcription factor controlling EMT initiation, Snail was found to be degraded by PS-T induced autophagy. In addition, overexpression of Snail reversed the inhibitory effects of PS-T. Furthermore, it was confirmed that the expression of Snail was inversely correlated with LC3 and associated with poor prognosis using immunohistochemistry and TCGA database analysis, respectively. Conclusions This study demonstrated that PS-T could inhibit EMT in breast cancer cells by inducing autophagy to degrade Snail protein, thus improving the prognosis of TNBC, offering potential treatment alternatives for TNBC patients.

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