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 TRPC6 Channels Are Required for Proliferation, Migration and Invasion of Breast Cancer Cell Lines by Modulation of Orai1 and Orai3 Surface Exposure

Cancers ◽  
2018 ◽  
Vol 10 (9) ◽  
pp. 331 ◽  
Author(s):  
Isaac Jardin ◽  
Raquel Diez-Bello ◽  
Jose Lopez ◽  
Pedro Redondo ◽  
Ginés Salido ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
Transient Receptor Potential Channels ◽  
Brdu Incorporation ◽  
Migration And Invasion ◽  
Breast Cancer Cell Lines ◽  
Mcf10a Cell

Transient receptor potential channels convey signaling information from a number of stimuli to a wide variety of cellular functions, mainly by inducing changes in cytosolic Ca2+ concentration. Different members of the TRPC, TRPM and TRPV subfamilies have been reported to play a role in tumorigenesis. Here we show that the estrogen receptor positive and triple negative breast cancer cell lines, MCF7 and MDA-MB-231, respectively, exhibit enhanced expression of the TRPC6 channel as compared to the non-tumoral MCF10A cell line. In vitro TRPC6 knockdown using shRNA impaired MCF7 and MDA-MB-231 cell proliferation, migration and invasion detected by BrdU incorporation, wound healing and Boyden chamber assays, respectively. Using RNAi-mediated TRPC6 silencing as well as overexpression of the pore-dead dominant-negative TRPC6 mutant we have found that TRPC6 plays a relevant role in the activation of store-operated Ca2+ entry in the breast cancer cell lines but not in non-tumoral breast cells. Finally, we have found that TRPC6 interacts with Orai1 and Orai3 in MCF7 and MDA-MB-231 cells and is required for the translocation of Orai1 and Orai3 to the plasma membrane in MDA-MB-231 and MCF7 cells, respectively, upon Ca2+ store depletion. These findings introduce a novel mechanism for the modulation of Ca2+ influx and the development of different cancer hallmarks in breast cancer cells.

Thirteen miRNAs involved in the response of breast cancer cells to doxorubicin.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e12019-e12019
Author(s):  
Eduardo Tormo ◽  
Begoña Pineda ◽  
Sandra Ballester ◽  
Octavio Burgues ◽  
Eva Serna ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Expression Profile ◽  
Mirna Expression ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Non Coding Rna ◽  
Mcf 7

e12019 Background: Mature microRNAs (miRNAs) are a class of naturally occurring, small non-coding RNA molecules, about 21–25 nucleotides. Growing evidence shows that miRNAs exhibit a variety of regulatory functions related to cell growth, development, and differentiation, and are associated with a wide variety of human diseases. Several miRNAs have been linked to cancer; since expression analysis studies have revealed perturbed miRNA expression in tumors compared to normal tissues. As a consequence, human miRNAs are likely to be highly useful as biomarkers, especially for future cancer diagnostics, and are emerging as targets for disease intervention. Since doxorubicin (DOX) has been used for a long time in breast cancer treatment, and resistance mechanisms are not clear understood, the aim of this work was to find a miRNA expression profile that could explain the regulation in different breast cancer cell lines under DOX treatment. Methods: Three breast cancer cell lines (MDA-MB-231, MDA-MB-468, and MCF-7) were cultured in normal conditions and also treated with DOX. Total RNA containing small non-coding RNA was isolated and its expression profile was performed by using GeneChip miRNA 2.0 array. Real time PCR validation was carried out to confirm the results. Results: Principal Component Analysis (PCA) of the small non-coding RNA profiles showed different expression patterns between normal conditions and DOX treatment in each cell line separately. Taken together in a Heat Map, miRNA expression profiles of MDA-MB-231 and MDA-MB-468 cell lines were closer in both normal and DOX treatment conditions, while miRNA expression profile of MCF-7 cell line showed strong differences. Total of 13 common miRNAs between the three cell lines were found to be significantly affected by DOX treatment. PCR validation confirmed the results obtained. Conclusions: We conclude that 13 common miRNAs are responsables of changes compared to treatment with DOX in breast cancer cell lines MDA-MB-231, MDA-MB-468 and MCF-7. This miRNAs are mainly related with cellular processes such as cell differentiation, vascularisation, apoptosis and cell proliferation and also involved in other cellular processes, such as cell migration.

Abstract 578: RARRES1 is a tumor suppressor in triple-negative breast cancer cell lines

2014 ◽  
Author(s):  
Krysta M. Coyle ◽  
Ahmad Vaghar-Kashani ◽  
Florence Wong ◽  
Cheryl Dean ◽  
Carman Giacomantonio ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines

TSGA10 Expression Status in Breast Cancer: The Role of Microenvironmental Changes

2020 ◽  
Author(s):  
Marzieh Marzbany ◽  
Amir Hossein Norooznezhad ◽  
Zohreh Hoseinkhani ◽  
Azadeh Mahnam ◽  
Kiumaras Eslampia ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Specific Gene ◽  
Mcf 7

Abstract Background: Testis-specific gene antigen (TSGA10) mainly involves in spermatogenesis and embryogenesis. In the new defined roles, being a tumor suppressor agent or a cancer/testis antigen (CTA) is still unclear for this protein. The current study aimed to examine exact role of TSGA10 as a tumor suppressor or CTA in breast cancer and evaluate the role of microenvironment on its expression. Methods: This study evaluated the expression of TSGA10 and hypoxia-inducible factor 1α (HIF-1α) in two different breast cancer cell lines (MCF-7 and MDA-MB23) as well as their control (MCF10A) using real-time PCR. Moreover, expression of the mentioned genes evaluated in samples obtained from tumoral tissues with two types of controls: paired (tumor-free margin) and unpaired (healthy individuals). Also, in order to asses TSGA10 levels in the tumoral tissues, western blotting was performed. Furthermore, to evaluate the role epigenetic changes on TSGA10 expression, breast cancer cell lines were treated with a histone deacetylase inhibitor (HDACI) as well as H2O2 for oxidative stress induction. Results: The current study evaluated 36 patients diagnosed with breast cancer as well as 10 healthy controls. According to the results, it was shown that 35 (97.7%) and 1 (2.8%) of patients were diagnosed with ductal and lobular carcinomas respectively. The TSGA10 levels in the tumoral samples showed 1.38±0.014-fold decrease and 1.41±0.127-fold increase compared with their paired (P<0.001) and unpaired (P<0.001) controls respectively. Moreover, results of blotting in tumoral tissues expressed significant decrease in TSGA10 levels in comparison to the paired controls (P<0.01). Among the cell lines, TSGA10 expression in MCF-7 and MDA-MB23 cells had 4.9±0.283 and 4.21±0.163 folds of decrease in normoxic and 4.7±.0.283 and 7.1±0.141 folds of expression reduction in hypoxic condition respectively (all P<0.0001). Furthermore, the results showed that HIF-1α expression was up-regulated in both normoxic (P<0.01) and hypoxic (P<0.01) conditions. Also, TSGA10 expression increased up to 7.39±0.156 folds in MCF-7 cells after HDACI treatment (all P<0.01). However, MDA-MB23 cells firstly experienced a decrease and then a notable increase in TSGA10 expression (all P<0.01). Conclusion: Results of current study showed that TSGA10 seems to be tumor suppressor, however, further studies are necessary.

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.

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