Effect of MicroRNA-150 (miR-150) on the Biological Activity of Breast Cancer Cells and Its Correlation with Notch Signal

2021 ◽  
Vol 11 (12) ◽  
pp. 2401-2406
Author(s):  
Jing Gao ◽  
Xiangchuan Liu ◽  
Huijuan Shi ◽  
Shugang Liu
Keyword(s):  
Breast Cancer ◽  
Biological Activity ◽  
Notch Signaling ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Mrna Levels ◽  
Pcr Cloning ◽  
Migration Ability ◽  
Group Ii ◽  
Mcf 7

Our study explores miR-150’s effect on the biological activity of breast cancer cells and its correlation with Notch signaling. Human breast cancer cells MCF-7 were divided into WZ group (MCF-7 cells); KZ group (transfected with miR-150-NC); and group II (transfected with miR-150inhibitor) followed by analysis of miR-150 expressio,n cell replication, apoptosis, invasion, migration ability and Notch1 and Notch3 expression by qRT-PCR, cloning, Hoechst33258 fluorescent staining, Transwell chamber, cell scratch test, dual luciferase report and Western blot. Lowest miR-150 expression in MCF-7 cells indicated a successful transfection (P < 0.05). Compared with KZ and WZ groups, Notch1 and Notch3 mRNA levels in group II were decreased (P <0.05); and the number of cell clones in group II was reduced (P <0.05) without difference between WZ and KZ group (P >0.05); miR-150 inhibitor reduced Notch1 and Notch3 expression (P <0.05). The fluorescence intensity of MCF-7 cells in group II was highest among three groups (P <0.05). The number of cell invasion and migration as well as Notch1 and Notch 3 expression in group II was reduced (P <0.05) without difference between group KZ and WZ (P >0.05). miR-150 expression is increased in MCF-7 cells. The miR-150 inhibitor can inhibit cell apoptosis, migration and other biological behaviors, which is related to target Notch signaling pathway.

scholarly journals Mummy Induces Apoptosis Through Inhibiting of Epithelial-Mesenchymal Transition (EMT) in Human Breast Cancer Cells

2020 ◽  
Vol 9 ◽  
pp. 1812
Author(s):  
Solmaz Rahmani Barouji ◽  
Arman Shahabi ◽  
Mohammadali Torbati ◽  
Seyyed Mohammad Bagher Fazljou ◽  
Ahmad Yari Khosroushahi
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Anticancer Activity ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Control Group ◽  
Mrna Levels ◽  
Mesenchymal Transition ◽  
Mcf 7

Background: Mummy (Iranian pure shilajit) is a remedy with possessing anti-inflammatory, antioxidant and anticancer activities. This study aimed to examine mummy effects on epithelial-mesenchymal transition (EMT) and invasiveness of MCF-7 and MDA-MB-231 breast cancer (BC) cell lines with underlying its mechanism. Materials and Methods: The dose-dependent inhibitory effect of the mummy on cell proliferation in vitro was determined using the MTT assay.  Flow cytometry and 4’,6-diamidino-2-phenylindole dihydrochloride staining were respectively used for quantitative and qualitative analysis of cellular apoptosis, and gene expression analysis was conducted using real-time PCR. Results: MDA-MB-231 showed more sensitivity than the MCF-7 cell line to the anticancer activity of mummy, while mummy did not exhibit significant cell cytotoxicity against human normal cells (MCF-10A). The gene expression profile demonstrated a significant decrease in TGF-β1, TGF-βR1, TWIST1, NOTCH1, CTNNB1, SRC along with an increase in E-cadherin mRNA levels in mummy treated cells compared to the untreated control group (P≤0.05). Conclusion: Mummy triggers inhibition of EMT and metastasis in breast cancer cells mainly through the downregulation of TGFβ1 activity, and more studies required to find its specific anticancer activity with details. [GMJ.2020;9:e1812]

Estrogen Activities and the Cellular Effects of Natural Progesterone from Wild Yam Extract in MCF-7 Human Breast Cancer Cells

2009 ◽  
Vol 37 (01) ◽  
pp. 159-167 ◽  
Author(s):  
Mi-Kyung Park ◽  
Hyeok-Yi Kwon ◽  
Woong-Shick Ahn ◽  
Sumi Bae ◽  
Mee-Ra Rhyu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Estrogenic Activity ◽  
Mrna Levels ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Wild Yam ◽  
Mcf 7

We studied the estrogenic activity and cellular effect of wild yam extract in MCF-7 human breast cancer cells. The extract increased the activity of the progesterone receptor and pS2 genes at the mRNA levels in human breast cancer MCF-7 cells, although the effects were not as prominent as those of 17β-estradiol (E2). Western blot analysis showed that the level of estrogen receptor α protein was down-regulated after treatment with E2 or wild yam extract. Wild yam extract also inhibited proliferation of MCF-7 cells. These data indicate that wild yam extract acts as a weak phytoestrogen and protects against proliferation in human breast carcinoma MCF-7 cells.

scholarly journals Evaluation of Potential Mechanisms Controlling the Catalase Expression in Breast Cancer Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Christophe Glorieux ◽  
Juan Marcelo Sandoval ◽  
Nicolas Dejeans ◽  
Sandrine Nonckreman ◽  
Khadija Bahloula ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Posttranslational Modifications ◽  
Breast Cancer Cells ◽  
Mammary Epithelial Cells ◽  
Dna Lesions ◽  
Mrna Levels ◽  
Chromosome 11 ◽  
Catalase Protein ◽  
Mcf 7

Development of cancer cell resistance against prooxidant drugs limits its potential clinical use. MCF-7 breast cancer cells chronically exposed to ascorbate/menadione became resistant (Resox cells) by increasing mainly catalase activity. Since catalase appears as an anticancer target, the elucidation of mechanisms regulating its expression is an important issue. In MCF-7 and Resox cells, karyotype analysis showed that chromosome 11 is not altered compared to healthy mammary epithelial cells. The genomic gain ofcatalaselocus observed in MCF-7 and Resox cells cannot explain the differential catalase expression. Since ROS cause DNA lesions, the activation of DNA damage signaling pathways may influence catalase expression. However, none of the related proteins (i.e., p53, ChK) was activated in Resox cells compared to MCF-7. The c-abl kinase may lead to catalase protein degradation via posttranslational modifications, but neither ubiquitination nor phosphorylation of catalase was detected after catalase immunoprecipitation. Catalase mRNA levels did not decrease after actinomycin D treatment in both cell lines. DNMT inhibitor (5-aza-2′-deoxycytidine) increased catalase protein level in MCF-7 and its resistance to prooxidant drugs. In line with our previous report, chromatin remodeling appears as the main regulator of catalase expression in breast cancer after chronic exposure to an oxidative stress.

scholarly journals Synthesis and Biological Activity of Diastereomeric and Geometric Analogs of Calcipotriol, PRI-2202 and PRI-2205, Against Human HL-60 Leukemia and MCF-7 Breast Cancer Cells

Cancers ◽  
2013 ◽  
Vol 5 (4) ◽  
pp. 1355-1378 ◽  
Author(s):  
Magdalena Milczarek ◽  
Michał Chodyński ◽  
Beata Filip-Psurska ◽  
Agnieszka Martowicz ◽  
Małgorzata Krupa ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Biological Activity ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Mcf 7

scholarly journals Increased 12-Lipoxygenase Expression in Breast Cancer Tissues and Cells. Regulation by Epidermal Growth Factor1

1997 ◽  
Vol 82 (6) ◽  
pp. 1790-1798 ◽  
Author(s):  
Rama Natarajan ◽  
Robert Esworthy ◽  
Wei Bai ◽  
Jia-Li Gu ◽  
Sharon Wilczynski ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Breast Cancer Cell Lines ◽  
Breast Epithelial Cell ◽  
Mrna Levels ◽  
Epidermal Growth ◽  
Mcf 7

Abstract The interaction of growth factors, such as epidermal growth factor (EGF) with their receptors, on breast cancer cells can lead to the hydrolysis of phospholipids and release of fatty acids, such as arachidonic acid, which can be further metabolized by the lipoxygenase (LO) pathway. Several LO products have been shown to stimulate oncogenes and have mitogenic and chemotactic effects. In this study, we have evaluated the regulation of 12-LO activity and expression in breast cancer cells and tissues. Leukocyte-type 12-LO messenger RNA (mRNA) expression was studied by a specific RT-PCR method in matched, normal, uninvolved and cancer-involved breast tissue RNA samples from six patients. In each of these six patients, the cancer-involved section showed a much higher level of 12-LO mRNA than the corresponding normal section. 12-LO mRNA levels also were greater in two breast cancer cell lines, MCF-7 and COH-BR1, compared with the nontumorigenic breast epithelial cell line, MCF-10F. The growth of the MCF-7 cells was significantly inhibited by two specific LO blockers but not by a cyclooxygenase blocker. Treatment of serum-starved MCF-7 cells with EGF for 4 h led to a dose-dependent increase in the formation of the 12-LO product, 12-hydroxyeicosatetraenoic acid. EGF treatment also increased the levels of the leukocyte-type 12-LO protein expression at 24 h. These results suggest that activation of the 12-LO pathway may play a key role in basal and EGF-induced breast cancer cell growth.

scholarly journals Induction of interferon-β and interferon signaling by TRAIL and Smac mimetics via caspase-8 in breast cancer cells

PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0248175
Author(s):  
Victoria Granqvist ◽  
Christian Holmgren ◽  
Christer Larsson
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Caspase 8 ◽  
Type I ◽  
Mrna Levels ◽  
Interferon Β ◽  
Er Positive ◽  
Smac Mimetics ◽  
Mcf 7

Breast cancer prognosis is frequently good but a substantial number of patients suffer from relapse. The death receptor ligand TRAIL can in combination with Smac mimetics induce apoptosis in some luminal-like ER-positive breast cancer cell lines, such as CAMA-1, but not in MCF-7 cells. Here we show that TRAIL and the Smac mimetic LCL161 induce non-canonical NF-κB and IFN signaling in ER-positive MCF-7 cells and in CAMA-1 breast cancer cells when apoptosis is blocked by caspase inhibition. Levels of p52 are increased and STAT1 gets phosphorylated. STAT1 phosphorylation is induced by TRAIL alone in MCF-7 cells and is independent of non-canonical NF-κB since downregulation of NIK has no effect. The phosphorylation of STAT1 is a rather late event, appearing after 24 hours of TRAIL stimulation. It is preceded by an increase in IFNB1 mRNA levels and can be blocked by siRNA targeting the type I IFN receptor IFNAR1 and by inhibition of Janus kinases by Ruxolitinib. Moreover, downregulation of caspase-8, but not inhibition of caspase activity, blocks TRAIL-mediated STAT1 phosphorylation and induction of IFN-related genes. The data suggest that TRAIL-induced IFNB1 expression in MCF-7 cells is dependent on a non-apoptotic role of caspase-8 and leads to autocrine interferon-β signaling.

scholarly journals 4sUDRB-sequencing for genome-wide transcription bursting quantification in breast cancer cells

2020 ◽  
Author(s):  
William F. Beckman ◽  
Miguel Ángel Lermo Jiménez ◽  
Perry D. Moerland ◽  
Hans V. Westerhoff ◽  
Pernette J. Verschure
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Burst Size ◽  
Mrna Levels ◽  
Gene Promoters ◽  
Genome Wide ◽  
A Genome ◽  
Mcf 7

AbstractEpigenetics maintains cell-identity specific gene-expression patterns. However, within a population of isogenic cells of the same identity, a substantial variability in gene expression and responsiveness is still observed. Transcription bursting is a substantial source of this gene-expression variability or ‘noise’, contributing to phenotypic heterogeneity and potentially driving both physiological and pathological processes such as differentiation or tumorigenesis and drug resistance. Identification of transcription-bursting dynamics at a genome-wide scale has been restricted to inferring bursts in mRNA production computationally from the heterogeneity of mRNA levels in single cell transcriptomic data. Systematic characterisation of the genomic and epigenetic chromatin context of genes with defined transcription bursting behaviour has been incomplete. Here, we measured the bursting of transcription itself by genome-wide nascent RNA sequencing of breast cancer MCF-7 cells upon synchronisation of transcription with a transcription elongation inhibitor and by calibration using live cell imaging of nascent PP7-tagged GREB1 transcription. Comparing across the entire genome, we find transcription bursting to be ubiquitous, with burst sizes of up to 160 transcripts. Transcription bursting attributes ~85% to a trend in the variation in steady state gene expression between genes, whereas both burst frequency and nascent transcript degradation attribute minimally. Individual genes deviate strongly from this trend and engage both in anomalous burst size and frequency. We find that the presence of the TATA box or Inr sequence within gene promoters significantly predicts a larger burst size, as do promoter-associated YY1 and E2F1 transcription-factor binding motifs. Enrichment of the transcription start site with epigenetic marks such as H3K79me2 and H3Kl4ac is also strongly associated with the transcription burst size. Finally, we show that in these MCF-7 breast-cancer cells, genes with a larger transcription burst size exhibit a larger immediate transcriptional response following endocrine drug treatment. Our genome-wide transcription-bursting analysis method paves the way to elucidate the dynamic role of epigenetic regulation on dynamic transcription in pathophysiology.

scholarly journals Role of specificity protein transcription factors in estrogen-induced gene expression in MCF-7 breast cancer cells

2007 ◽  
Vol 39 (4) ◽  
pp. 289-304 ◽  
Author(s):  
Shaheen Khan ◽  
Fei Wu ◽  
Shengxi Liu ◽  
Qian Wu ◽  
Stephen Safe
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Retinoic Acid Receptor ◽  
Estrogen Receptor Α ◽  
Mrna Levels ◽  
Aspartate Transcarbamylase ◽  
Mcf 7

AbstractDeletion analysis of several 17β-estradiol (E2)-responsive genes have identified GC-rich sites that are associated with hormone-induced transactivation in MCF-7 breast cancer cells. However, the role of individual specificity proteins (Sps) in mediating hormone-induced gene expression has not been unequivocally determined. In transient transfection studies using E2-responsive GC-rich promoters from the E2F1, carbamoylphosphate synthetase/aspartate transcarbamylase/dihydroorotase (CAD), and retinoic acid receptor α (RARα) genes, RNA interference using small inhibitory RNAs for Sp1 (iSp1), Sp3 (iSp3), and Sp4 (iSp4) decreased both basal and E2-induced transactivation. The contributions of individual Sp proteins to basal and E2-induced activity were promoter dependent. iSp1, iSp3, and iSp4 also significantly inhibited hormonal induction of E2F1, CAD, and RARα mRNA levels; however, the enhanced inhibitory effects of the latter two small inhibitory RNAs suggest that Sp3 and Sp4 play a major role in estrogen receptor α/Sp-mediated gene expression in MCF-7 cells.

scholarly journals Biochanin A Promotes Proliferation that Involves a Feedback Loop of MicroRNA-375 and Estrogen Receptor Alpha in Breast Cancer Cells

2015 ◽  
Vol 35 (2) ◽  
pp. 639-646 ◽  
Author(s):  
Jian Chen ◽  
Bo Ge ◽  
Yong Wang ◽  
Yu Ye ◽  
Sien Zeng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Feedback Loop ◽  
Biochanin A ◽  
Mrna Levels ◽  
Mcf 7

Background: Biochanin A and formononetin are O-methylated isoflavones that are isolated from the root of Astragalus membranaceus, and have antitumorigenic effects. Our previous studies found that formononetin triggered growth-inhibitory and apoptotic activities in MCF-7 breast cancer cells. We performed in vivo and in vitro studies to further investigate the potential effect of biochanin A in promoting cell proliferation in estrogen receptor (ER)-positive cells, and to elucidate underlying mechanisms. Methods: ERα-positive breast cancer cells (T47D, MCF-7) were treated with biochanin A. The MTT assay and flow cytometry were used to assess cell proliferation and apoptosis. mRNA levels of ERα, Bcl-2, and miR-375 were quantified using real-time polymerase chain reaction. Compared with the control, low biochanin A concentrations (2-6 μM) stimulated ERα-positive cell proliferation (T47D, MCF-7). The more sensitive T47D cells were used to study the relevant signaling pathway. Results: After treatment with biochanin A, ERα, miR-375, and Bcl-2 expression was significantly upregulated. Additionally, in the in vivo studies, uterine weight in ovariectomized mice treated with biochanin A increased significantly. Conclusion: This study demonstrated that biochanin A promoted ERα-positive cell proliferation through miR-375 activation and this mechanism is possibly involving in a miR-375 and ERα feedback loop.

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