scholarly journals Caveolin 1 knockdown inhibits the proliferation, migration and invasion of human breast cancer BT474 cells

2014 ◽  
Vol 9 (5) ◽  
pp. 1723-1728 ◽  
Author(s):  
RUI WANG ◽  
ZHI LI ◽  
HUI GUO ◽  
WEI SHI ◽  
YUE XIN ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Migration And Invasion ◽  
Human Breast ◽  
Caveolin 1

scholarly journals Antiproliferative Activity of Combined Biochanin A and Ginsenoside Rh2 on MDA-MB-231 and MCF-7 Human Breast Cancer Cells

Molecules ◽  
2018 ◽  
Vol 23 (11) ◽  
pp. 2908 ◽  
Author(s):  
Guixing Ren ◽  
Zhenxing Shi ◽  
Cong Teng ◽  
Yang Yao
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Human Breast Cancer ◽  
Synergistic Effects ◽  
Inhibitory Effect ◽  
Biochanin A ◽  
Migration And Invasion ◽  
Ginsenoside Rh2 ◽  
Human Breast ◽  
Mcf 7

Breast cancer is the most frequently diagnosed cancer in women worldwide. The antiproliferative activities of biochanin A (BA) and ginsenoside Rh2 were determined by evaluating their inhibitory effect on MDA-MB-231 human breast cancer cell proliferation. The combination of BA with Rh2 was also assessed. In MDA cells, combination treatment led to a decrease in the EC50 values of BA and Rh2 to 25.20 μM and 22.75 μM, respectively. In MCF-7 cells, the EC50 values of combined BA and Rh2 decreased to 27.68 μM and 25.41 μM, respectively. BA combined with Rh2 also improved the inhibition of MDA-MB-231 and MCF-7 cell migration and invasion compared to the individual compounds. Western blot analysis demonstrated upregulation in p-p53, p-p38, and p-ASK1 proteins while levels of TRAF2 were downregulated. These results suggest that BA combined with Rh2 exhibits synergistic effects against MDA-MB-231 and MCF-7 cell proliferation.

scholarly journals Tumor suppressive function of Matrin 3 in the basal-like breast cancer

2020 ◽  
Vol 53 (1) ◽  
Author(s):  
Jaehyuk Yang ◽  
Seung Jun Lee ◽  
Yongseok Kwon ◽  
Li Ma ◽  
Jongchan Kim
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Patient Survival ◽  
Apoptotic Cell ◽  
Migration And Invasion ◽  
Breast Cancer Patients ◽  
Human Breast ◽  
Basal Like Breast Cancer ◽  
Tumor Suppressive Function

Abstract Background Basal-like breast cancer (BLBC) or triple-negative breast cancer (TNBC) is an aggressive and highly metastatic subtype of human breast cancer. The present study aimed to elucidate the potential tumor-suppressive function of MATR3, an abundant nuclear protein, in BLBC/TNBC, whose cancer-relevance has not been characterized. Methods We analyzed in vitro tumorigenecity by cell proliferation and soft agar colony formation assays, apoptotic cell death by flow cytometry and Poly (ADP-ribose) polymerase (PARP) cleavage, epithelial-mesenchymal transition (EMT) by checking specific EMT markers with real-time quantitative PCR and in vitro migration and invasion by Boyden Chamber assays. To elucidate the underlying mechanism by which MATR3 functions as a tumor suppressor, we performed Tandem affinity purification followed by mass spectrometry (TAP-MS) and pathway analysis. We also scrutinized MATR3 expression levels in the different subtypes of human breast cancer and the correlation between MATR3 expression and patient survival by bioinformatic analyses of publicly available transcriptome datasets. Results MATR3 suppressed in vitro tumorigenecity, promoted apoptotic cell death and inhibited EMT, migration, and invasion in BLBC/TNBC cells. Various proteins regulating apoptosis were identified as MATR3-binding proteins, and YAP/TAZ pathway was suppressed by MATR3. MATR3 expression was inversely correlated with the aggressive and metastatic nature of breast cancer. Moreover, high expression levels of MATR3 were associated with a good prognosis of breast cancer patients. Conclusions Our data demonstrate that MATR3 functions as a putative tumor suppressor in BLBC/TNBC cells. Also, MATR3 potentially plays a role as a biomarker in predicting chemotherapy-sensitivity and patient survival in breast cancer patients.

scholarly journals Clinical significance of Caveolin-1, Caveolin-2 and HER2/neu mRNA expression in human breast cancer

2004 ◽  
Vol 91 (5) ◽  
pp. 959-965 ◽  
Author(s):  
Y Sagara ◽  
K Mimori ◽  
K Yoshinaga ◽  
F Tanaka ◽  
K Nishida ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mrna Expression ◽  
Clinical Significance ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Caveolin 1

Long Noncoding RNA LINC00261 Induces Chemosensitization to Tamoxifen in Human Breast Cancer

2020 ◽  
Vol 10 (6) ◽  
pp. 789-797
Author(s):  
Zhaoyan Shi ◽  
Weidong Xiao ◽  
Meifang Hu
Keyword(s):  
Breast Cancer ◽  
Protein Expression ◽  
Human Breast Cancer ◽  
Noncoding Rna ◽  
Quantitative Polymerase Chain Reaction ◽  
Chemotherapy Resistance ◽  
Migration And Invasion ◽  
Human Breast ◽  
Mcf 7

Breast cancer (BC) is one of the most prevalent and mortal malignancies in women worldwide, and tamoxifen is the mainstay treatment of breast cancer and the development of resistance represents a major obstacle for a cure. Long non-coding RNAs (LncRNAs) LINC00261 have been identified to serve a key role in the development of several tumors. However, the role of LINC00261 in breast cancer and chemotherapy resistance remains largely unknown. To investigate the role of LINC00261 in BC cells, LINC00261 was upregulated in MCF-7-TAM cells by transfecting with LINC00261 plasmid (pcDNA-LINCC00261). Subsequently, cell viability and drug sensitivity were measured using the CCK-8 assay. Reverse transcription-quantitative polymerase chain reaction (qRT-PCR) was performed to detect the level of LINC00261 in BC cells. Cell migration, invasion, and apoptosis were detected by Transwell, Scratch Test and Flow cytometry, respectively. Additionally, the associated protein expression was detected using Western blot. The results demonstrated that LINC00261 was significantly down-regulated in BC cells, especially in MCF-7-TAM cells. Overexpression of LINC00261 inhibited cell proliferation, migration, and invasion in MCF-7-TAM cells. Further, an abundant of LINC00261 sensitized breast cancer cells to tamoxifen and reduced tamoxifen-induced apoptosis in MCF-7-TAM cells. Finally, LINC00261 significantly regulated the protein expression of drug-resistant genes and the protein expression related to tumor metastasis and cell apoptosis. Therefore, this study revealed that LINC00261 induces chemosensitization to tamoxifen in human breast cancer, it may be a useful biomarker and potential therapeutic target.

scholarly journals MiR-410 Acts as a Tumor Suppressor in Estrogen Receptor-Positive Breast Cancer Cells by Directly Targeting ERLIN2 via the ERS Pathway

2018 ◽  
Vol 48 (2) ◽  
pp. 461-474 ◽  
Author(s):  
Hewen Wu ◽  
Junli Li ◽  
En’en Guo ◽  
Suxia Luo ◽  
Guohui Wang
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Endoplasmic Reticulum ◽  
Estrogen Receptor ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Migration And Invasion ◽  
Human Breast ◽  
Er Positive ◽  
Positive Breast Cancer

Background/Aims: Endoplasmic reticulum lipid raft-associated 2 (ERLIN2) is reported to be overexpressed in human breast cancer cells and plays an important role in cell proliferation. MicroRNAs (miRNAs) act as post-transcriptional regulators of gene expression and are involved in the development of multiple malignancies, including breast cancer. However, the molecular mechanism of the aberrant ERLIN2 expression in human breast cancer remains poorly understood. Methods: MiR-410 expression level was analyzed using Real-time PCR, and ERLIN2 expression was analyzed using Western blot, Real-time PCR and immunohistochemical staining. The effect of miR-410 on ERLIN2 3’UTR intensity was performed using a luciferase assay. Cell proliferation was analyzed using CCK-8 and colony formation assay, together with an Annexin V-PE/7-AAD kit for cell apoptosis assay. Cell migration and invasion was detected using a Transwell migration and invasion assay. Methylation specific PCR was used to examine whether miR-410 promoter was demethylated. Results: In this study, we validated that ERLIN2 was a direct target of miR-410 and miR-410 suppressed ERLIN2 expression at the post-transcriptional level. Importantly, the regulation of ERLIN2 by miR-410 was estrogen receptor (ER) dependent. Functional studies demonstrated that miR-410 inhibited breast cancer cell proliferation, migration and invasion, but promoted cell apoptosis. However, inhibition of miR-410 resulted in opposite effects. A xenograft nude mouse model further confirmed that miR-410 suppressed breast tumor growth. In addition, miR-410 modulated the expression levels of epithelial-mesenchymal transition (EMT)-related genes. ERLIN2 knockdown suppressed cell proliferation, migration and invasion, as well as EMT. ERLIN2 overexpression can restore the cell proliferation, migration and invasion that were inhibited by miR-410. Furthermore, our data demonstrated that miR-410 inhibition suppressed the expression of endoplasmic reticulum-stress (ERS)-related genes, while ERLIN2 knockdown abrogated the effects of miR-410 inhibitor. Finally, we showed that miR-410 was downregulated in human ER-positive breast cancer tissues, inversely correlated with ERLIN2. We further demonstrated the downregulation of miR-410 in breast cancer might be due to the hypermethylation of its promoter. Conclusions: Our study indicates that miR-410 suppresses cell growth, migration and invasion by directly downregulating ERLIN2 in ER positive breast cancer, acting as a tumor suppressor. Our study also suggests that miR-410 may serve as a potential therapeutic target for patients with ER positive breast cancer.

Sign in / Sign up

Export Citation Format

Share Document