scholarly journals LncRNA MIR4435-2HG Promotes Proliferation, Migration, Invasion and EMT Via Targeting miR-22- 3p/TMEM9B in Breast Cancer

2021 ◽  
Author(s):  
Jing Ke ◽  
Quhui Wang ◽  
Wei Zhang ◽  
Haijun Mei
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
Luciferase Reporter ◽  
Breast Cancer Cell Lines ◽  
Reporter Assay ◽  
Cancer Tissues ◽  
Dual Luciferase Reporter Assay

Abstract Background: Breast cancer, as the malignancy with the highest incidence rate and mortality rate in women, seriously threatens human life and health. Pieces of evidence have suggested that long non-coding RNAs (lncRNAs) possess important effects on regulating the occurrence and development of breast cancer.Results: In the present study, MIR4435-2HG was highly expressed in breast cancer tissues and cells. Down-regulation of MIR4435-2HG inhibited the viability, proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of breast cancer cell lines by Cell Counting Kit-8 (CCK-8), colony formation, transwell migration and invasion, immunofluorescence and western blot assays. Dual-luciferase reporter assay and RNA pull-down analysis confirmed that miR-22-3p was a target of MIR4435-2HG. Over-expression of MicroRNA-22-3p (miR-22-3p) obviously inhibited the viability, proliferation, migration, invasion and EMT of breast cancer cell lines. Transmembrane protein 9 domain family member B (TMEM9B) was up-regulated in breast cancer tissues and cell lines. Dual-luciferase reporter assay confirmed that TMEM9B was a target of miR-22-3p. TMEM9B inhibition partially restored the effects of MIR4435-2HG/miR-22-3p on the viability, proliferation, migration, invasion and EMT of breast cancer cell lines.Conclusions: MIR4435-2HG potentially played a tumor-promoting role in the occurrence and development of breast cancer, which might be achieved by regulating the miR-22-3p/TMEM9B axis.

Effect of MiR-137 and MiR-496 on Del-1 and triple negative breast cancer progression.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e23058-e23058
Author(s):  
Jae-Hwan Jeong ◽  
Soo Jung Lee ◽  
Jeeyeon Lee ◽  
Jin Hyang Jung ◽  
Ho Yong Park ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Progression ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Cancer Cell Lines ◽  
Luciferase Reporter ◽  
Breast Cancer Cell Lines

e23058 Background: Although Del-1 was recently proposed as a new biomarker for early breast cancer in our previous studies, the mechanisms of Del-1 expression are barely understood. In the current study, we selected two microRNAs (miR-137 and - 496), potentially affecting Del-1 expression in breast cancer and examined their impact on Del-1 expression in a variety of breast cancer cell lines to identify their potential role in Del-1 expression and thereby breast cancer development or progression. . Methods: Del-1 mRNA and miR-137/– 496 levels were measured by qRT-PCR among breast epithelial (MCF10A) and cancer cells (MDA-MB-231, MCF7, SK-BR3 and T-47D). The effects of miR-137/– 496 on cell proliferation and invasion were detected using MTT, wound healing and Transwell assays. Furthermore, luciferase reporter assay was used to identify the direct regulation of Del-1 by miR-137 or – 496 in MDA-MB-231 cells. Plus, we analyzed the expressions of miR-137 or – 496 and Del-1 mRNA from 20 patients with triple negative early breast cancer. Results: miR-137 and – 496 levels were low in all breast cancer cell lines. As Del-1 mRNA expression was remarkably higher in MDA-MB-231 compared to the other breast cancer cell lines, further functional analyses were done with MDA-MB-231 representing triple negative breast cancer subtype. Both miR-137 and miR-496 were revealed to directly bind at the 3’-UTR of Del-1. Del-1 by Luciferase reporter assay and Del-1 expression was upregulated by inhibitors and reversed by both mimics of both miR-137 and miR-496. Furthermore, both miR-137 and miR-496 were also demonstrated to inhibit cell proliferation, migration and invasion of MDA-MB-231, suggesting that these miRNAs affect cancer progression via Del-1. MiR-137 and miR-496 were remarkably down-regulated in 7 out of 12 triple negative breast cancer tissues, in particular with high Ki67 and high histologic grade. Conclusions: Although Del-1 was recently introduced as a new biomarker for triple negative breast cancer, the mechanisms of Del-1 expression were barely identified. The current study firstly demonstrated that microRNA 137 and 496 are involved in Del-1 regulation by binding at Del-1 gene, affecting cancer progression by altering Del-1 expression.

scholarly journals SOX9 is a Target of miR-134-3p And miR-224-3p in Beast Cancer Cell Lines

2021 ◽  
Author(s):  
Tsu-Yang Chao ◽  
Theresa Kordaß ◽  
Wolfram Osen ◽  
Stefan B. Eichmüller
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Progression ◽  
Cancer Cell Lines ◽  
Luciferase Reporter ◽  
Breast Cancer Cell Lines ◽  
Sox9 Expression ◽  
Reporter Assays

Abstract SOX9 represents a transcription factor identified as an important mediator of cancer progression in breast cancer. miRNAs are small non-coding RNAs that can inhibit translation of target genes by binding to the 3’-UTR region of the respective mRNA molecule. Deregulated miRNA expression plays a pivotal role in hallmarks of cancer such as sustained proliferation and inhibition of apoptosis. In this study we investigated the miRNA-mediated regulation of SOX9 expression in two breast cancer cell lines providing further insights into cellular mechanisms driving breast cancer progression. The effect of miR-134-3p, miR-224-3p and miR-6859-3p on SOX9 expression was tested on mRNA as well as protein level in the human breast cancer cell line MDA-MB-231. Furthermore, direct binding of these miRNAs to the SOX9 3’-UTR was assessed by luciferase reporter assays and site-directed mutagenesis in MDA-MB-231 and MCF-7 cells. SOX9 expression was significantly reduced on mRNA and protein level by transfection of either miR-134-3p, miR-224-3p or miR-6859-3p. Luciferase reporter assays proved direct binding of miR-134-3p and miR-224-3p to the SOX9 3’-UTR in MDA-MB-231 and MCF-7 cells. Expression analysis performed in silico revealed reduced expression of both miRNAs in breast cancer tissues. We describe three novel miRNAs capable of targeting SOX9 in human breast cancer cell lines. For miR-134-3p and miR-224-3p direct interaction with the SOX9 3’-UTR was proven. Furthermore, miR-134-3p and miR-224-3p reduced breast cancer cell viability, which is in line with the tumorigenic effects reported for SOX9 in breast cancer.

The novel long non-coding RNA PANCR: A p53 activator and potential breast cancer biomarkers.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e23016-e23016
Author(s):  
Yu Cao ◽  
Deliang Cao ◽  
Hongyan Ling
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Mcf10a Cell ◽  
Non Coding Rna ◽  
Cancer Tissues

e23016 Background: Long non-coding RNAs (LncRNAs) may serve as a biomarker and potential therapeutic target of cancers. Chromosome 16q22.1 is frequently deleted in breast cancer and may contribute to breast carcinogenesis by inactivation of tumor suppressor genes. This study characterized a new LncRNA tumor suppressor in this region, named p53 activating non-coding RNA (PANCR). This LncRNA consists of 1.5kb in length. Methods: Quantitative real-time PCR was used for examine the PANCR expression in breast cancer tissues. RNA-pull down and RNA-Immunopreicitation were used to analyze PANCR targeted protein. Results: Our data showed that PANCR was downregulated in breast cancer cell lines and tissues. In the breast cancer cell lines, PANCR expression appeared reversely correlated with cell malignancy, and in breast cancer tissues, PANCR was downregulated over 2 times in 31(62.0%) of 50 cases compared to adjacent normal breast tissues. In breast cancer cells MCF7 and immortalized human mammary epithelial cells MCF10A, ectopic expression of PANCR induced marked apoptosis, suppressing cell proliferation in culture and tumor growth in xenografts, but in contrast, shRNA–mediated silencing of PANCR promoted cell growth and proliferation. Mechanistic approaches revealed that in both MCF7 and MCF10A cell, PANCR activated p53 and upregulated pro-apoptotic proteins bid and bim and cell cycle inhibitors p21waf/cip1 and p27Kip1. We further found that the PANCR binds to and activates p53 by dissociating the p53-MDM2 complex. We further characterized the functional domain of PANCR that interacts with p53. Conclusions: The LncRNA PANCR located in the deleted Chromosome 16q22.1 region is a novel intracellular p53 activator and tumor suppressor, which may be used as a target for cancer therapy through mimicking its binding domain and activation of p53.

scholarly journals Increased expression of MUSASHI1 in epithelial breast cancer cells is due to down regulation of miR-125b

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Mahboobeh Forouzanfar ◽  
Liana Lachinani ◽  
Kianoush Dormiani ◽  
Mohammad Hossein Nasr-Esfahani ◽  
Kamran Ghaedi
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cells ◽  
Cancer Cell Lines ◽  
Luciferase Reporter ◽  
Breast Cancer Cell Lines ◽  
Oncogenic Protein ◽  
Cancer Tissues

Abstract Background Musashi1 (MSI1) is an oncogenic protein with a crucial role in the proliferation and characteristics of the epithelial cells in breast cancer. The change in expression of MSI1 has a role in solid tumor progression. There are different factors that regulate MSI1 expression in various cancer tissues including microRNAs which are considered as one of the most important of these factors. The aim of our study is identification of the molecular cause of maximal expression of MSI1 in epithelial breast cancer cell lines. Results Among predicted microRNAs, miR-125b, miR-637 and miR-802 were able to significantly reduce the luciferase activity. In addition, the relative expression of these three miRNAs were measured in the cancerous cell lines that results showed a significant reduction in expression of all microRNAs. On the other hand, only the overexpression of miR-125b caused a change in the expression pattern of MSI1 in breast epithelial cancer cell lines. Accordingly, our results demonstrated that the exogenous expression of miR-125b decreased not only the MSI1 protein but also expression of epithelial markers in breast cancer cells. Conclusions The results of luciferase reporter assay showed that MSI1 is a direct target for miR-125b in epithelial breast cancer cells. Moreover, higher amount of MSI1 in those cell lines seems due to the reduced amount of miR-125b, which is responsible for epithelial features of those kinds of cancer cells. Therefore, the modulation of miR-125b may be a potential approach to help to combat against epithelial breast tumors.

Cytotoxic activity and anti-cancer potential of Ontario grown onion extracts against breast cancer cell lines

2018 ◽  
Vol 8 (3) ◽  
pp. 159 ◽  
Author(s):  
Meghan Fragis ◽  
Abdulmonem I. Murayyan ◽  
Suresh Neethirajan
Keyword(s):  
Breast Cancer ◽  
Cytotoxic Activity ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Cytotoxic Activities ◽  
Cancer Line ◽  
Mcf 7

Background: Breast cancer is the most commonly diagnosed cancer and the second leading cause of cancer deaths among Canadian women. Cancer management through changes in lifestyle, such as increased intake of foods rich in dietary flavonoids, have been shown to decrease the risk associated with breast, liver, colorectal, and upper-digestive cancers in epidemiologic studies. Onions are high in flavonoid content and one of the most common vegetables. Additionally, onions are used in most Canadian cuisines.Methods: We investigated the effect of five prominent Ontario grown onion (Stanley, Ruby Ring, LaSalle, Fortress, and Safrane) extracts on two subtypes of breast cancer cell lines: a triple negative breast cancer line MDA-MB-231 and an ER+ breast cancer line MCF-7.Results: These onion extracts elicited strong anti-proliferative, anti-migratory, and cytotoxic activities on both the cancer cell lines. Flavonoids present in these onion extracts induced apoptosis, cell cycle arrest in the G2/M phase, and a reduction in mitochondrial membrane potential at dose-dependent concentrations. Onion extracts were more effective against MDA-MB-231 compared to the MCF-7 cell line. Conclusion: In this study, we investigated the extracts synthesized from Ontario-grown onion varieties in inducing anti-migratory, cytostatic, and cytotoxic activities in two sub-types of human breast cancer cell lines. Anti-tumor activity of these extracts depends upon the varietal and can be formulated into nutraceuticals and functional foods for the wellbeing of cancer patients. Overall, the results suggest that onion extracts are a good source of flavonoids with anti-cancerous properties.Keywords: onion extracts; flavonoids; anti-proliferative; breast cancer; cytotoxic activity

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