scholarly journals MicroRNA-137 Inhibits Cancer Progression by Targeting Del-1 in Triple-Negative Breast Cancer Cells

2019 ◽  
Vol 20 (24) ◽  
pp. 6162 ◽  
Author(s):  
Soo Jung Lee ◽  
Jae-Hwan Jeong ◽  
Seung Hee Kang ◽  
Jieun Kang ◽  
Eun Ae Kim ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mirna Regulation

MicroRNAs (miRNAs) can be used to target a variety of human malignancy by targeting their oncogenes or tumor suppressor genes. The developmental endothelial locus-1 (Del-1) might be under miRNA regulation. This study investigated microRNA-137 (miR-137) function and Del-1 expression in triple-negative breast cancer (TNBC) cells and tissues. Del-1 mRNA and miRNA-137 levels were determined via qRT-PCR in breast cancer cells (MDA-MB-231, MCF7, SK-BR3, and T-47D) and tissues from 30 patients with TNBC. The effects of miR-137 on cell proliferation, migration, and invasion were determined using MTT assays, wound healing, and Matrigel transwell assays. The luciferase reporter assay revealed direct binding of miR-137 to the 3′-UTR of Del-1. miR-137 inhibited cell proliferation, migration, and invasion of MDA-MB-231 cells. Among the 30 TNBC specimens, miR-137 was downregulated and Del-1 level in plasma was significantly elevated relative to normal controls. It is concluded that miR-137 regulates Del-1 expression in TNBC by directly binding to the Del-1 gene and cancer progression. The results implicate miR-137 as a new therapeutic biomarker for patients with TNBC.

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.

scholarly journals Kdm4c is Recruited to Mitotic Chromosomes and Is Relevant for Chromosomal Stability, Cell Migration and Invasion of Triple Negative Breast Cancer Cells

2018 ◽  
Vol 12 ◽  
pp. 117822341877307 ◽  
Author(s):  
Jeison Garcia ◽  
Fernando Lizcano
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Cancer Cell Line ◽  
Migration And Invasion ◽  
Mitotic Chromosomes ◽  
Lysine Demethylase

Members of the jumonji-containing lysine demethylase protein family have been associated with cancer development, although their specific roles in the evolution of tumor cells remain unknown. This work examines the effects of lysine demethylase 4C (KDM4C) knockdown on the behavior of a triple-negative breast cancer cell line. KDM4C expression was knocked-down by siRNA and analyzed by Western blot and immunofluorescence. HCC38 cell proliferation was examined by MTT assay, while breast cancer cells’ migration and invasion were tested in Transwell format by chemotaxis. Immunofluorescence assays showed that KDM4C, which is a key protein for modulating histone demethylation and chromosome stability through the distribution of genetic information, is located at the chromosomes during mitosis. Proliferation assays demonstrated that KDM4C is important for cell survival, while Transwell migration and invasion assays indicated that this protein is relevant for cancer progression. These data indicate that KDM4C is relevant for breast cancer progression and highlight its importance as a potential therapeutic target.

scholarly journals The inhibitory effects of butein on cell proliferation and TNF-α-induced CCL2 release in racially different triple negative breast cancer cells

PLoS ONE ◽  
2019 ◽  
Vol 14 (10) ◽  
pp. e0215269
Author(s):  
Patricia Mendonca ◽  
Ainsley Horton ◽  
David Bauer ◽  
Samia Messeha ◽  
Karam F. A. Soliman
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Inhibitory Effects ◽  
Tnf Α

scholarly journals STAT3 Targets ERR-α to Promote Epithelial–Mesenchymal Transition, Migration, and Invasion in Triple-Negative Breast Cancer Cells

2019 ◽  
Vol 17 (11) ◽  
pp. 2184-2195 ◽  
Author(s):  
Jia-Hui Ma ◽  
Jie Qi ◽  
Shi-Qi Lin ◽  
Cai-Yun Zhang ◽  
Fang-yuan Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Mesenchymal Transition

miR-103 regulates triple negative breast cancer cells migration and invasion through targeting olfactomedin 4

2017 ◽  
Vol 89 ◽  
pp. 1401-1408 ◽  
Author(s):  
Bin Xiong ◽  
Xuefeng Lei ◽  
Lei Zhang ◽  
Jia Fu
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Migration And Invasion

scholarly journals MiR-212-5p Suppresses the Epithelial-Mesenchymal Transition in Triple-Negative Breast Cancer by Targeting Prrx2

2017 ◽  
Vol 44 (5) ◽  
pp. 1785-1795 ◽  
Author(s):  
Zhi-Dong Lv ◽  
Dong-Xia Yang ◽  
Xiang-Ping Liu ◽  
Li-Ying Jin ◽  
Xin-Gang Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Ectopic Expression ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Lymph Node Status ◽  
Mesenchymal Transition ◽  
Expression Levels

Background/Aims: Triple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype. Our study investigated the functional role of miR-212-5p in TNBC. Methods: Realtime PCR was used to quantify miR-212-5p expression levels in 30 paired TNBC samples and adjacent normal tissues. Wound healing and Transwell assays were used to evaluate the effects of miR-212-5p expression on the invasiveness of TNBC cells. Luciferase reporter and Western blot assays were used to verify whether the mRNA encoding Prrx2 is a major target of miR-212-5p. Results: MiR-212-5p was downregulated in TNBC, and its expression levels were related to tumor size, lymph node status and vascular invasion in breast cancer. We also observed that the miR-212-5p expression level was significantly correlated with a better prognosis in TNBC. Ectopic expression of miR-212-5p induced upregulation of E-cadherin expression and downregulation of vimentin expression. The expression of miR212-5p also suppressed the migration and invasion capacity of mesenchymal-like cancer cells accompanied by a morphological shift towards the epithelial phenotype. Moreover, our study observed that miR-212-5p overexpression significantly suppressed Prrx2 by targeting its 3’-untranslated region (3’-UTR) region, and Prrx2 overexpression partially abrogated miR-212-5p-mediated suppression. Conclusions: Our study demonstrated that miR-212-5p inhibits TNBC from acquiring the EMT phenotype by downregulating Prrx2, thereby inhibiting cell migration and invasion during cancer progression.

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