scholarly journals VSP‑17 suppresses the migration and invasion of triple‑negative breast cancer cells through inhibition of the�EMT process via the PPARγ/AMPK signaling pathway

2020 ◽  
Author(s):  
Xiaotian Xu ◽  
Meng Liu ◽  
Yingying Yang ◽  
Chengqiong Wei ◽  
Xiyang Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Migration And Invasion ◽  
Ampk Signaling

Naringin inhibits growth potential of human triple-negative breast cancer cells by targeting β-catenin signaling pathway

2013 ◽  
Vol 220 (3) ◽  
pp. 219-228 ◽  
Author(s):  
Hongzhong Li ◽  
Bing Yang ◽  
Jing Huang ◽  
Tingxiu Xiang ◽  
Xuedong Yin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Growth Potential

scholarly journals Shikonin inhibits migration and invasion of triple-negative breast cancer cells by suppressing epithelial-mesenchymal transition via miR-17-5p/PTEN/Akt pathway

2020 ◽  
Author(s):  
Chang Bao ◽  
Tao Liu ◽  
Lingbo Qian ◽  
Chi Xiao ◽  
Xinru Zhou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Luciferase Reporter ◽  
Akt Pathway ◽  
Migration And Invasion ◽  
Pathway Enrichment Analysis ◽  
Mesenchymal Transition

Abstract Background: Triple-negative breast cancer(TNBC) is a great threat to global women’s health due to its high metastatic potential. Epithelial-to-mesenchymal transition (EMT) is considered as a key event in the process of metastasis. So the pharmacological targeting of EMT might be a promising strategy in improving the therapeutic efficacy of TNBC. Here, we investigated the effect of shikonin exerting on EMT and consequently the metastasis of TNBC cells and its underlying mechanism.Methods: The invasive and migratory capacities of MDA-MB-231 cells were tested using transwell invasion and wound healing assay. MiR-17-5p expression was examined by qRT-PCR. MiR-17-5p targeted genes were predicted with different bioinformatic algorithms from four databases (TargetScan, miRanda, PITA and picTar) and further screened by KEGG pathway enrichment analysis. The differential expressions of predicted genes and their correlations with miR-17-5p were identifed in breast cancer patients based on The Cancer Genome Atlas (TCGA) database. The interaction between PTEN and miR-17-5p was analyzed by luciferase reporter assay. The overexpression vector and small interfering RNA were constructed to investigate the role PTEN played in matastasis and EMT regulation. The expressions of EMT markers, Akt and p-Akt were evaluated by western blot.Results: Shikonin inhibited the migration and invasion of MDA-MB-231 cells by suppressing EMT. Shikonin suppressed the expression of miR-17-5p, which was upregulated in breast cancer and promoted cancer cell migration, invasion and EMT. The 3’-untranslated region of PTEN was found to be direct binding target of miR-17-5p. PTEN expression increased or decreased in breast cancer cells transfected with miR-17-5p inhibitors or mimics respectively. PTEN functioned as a suppressor both in the metastasis and EMT of TNBC cells. Overexpression or knockdown of PTEN reduced or increased the Akt and p-Akt expression respectively.Conclusions: Shikonin inhibits migration and invasion of TNBC cells by suppressing EMT via miR-17-5p/PTEN/Akt pathway. This suggests shikonin as a promising therapeutic agent to counteract metastasis in the TNBC patients.

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