Detection of miRNA in Cultured Cells or Xenograft Tissues of Breast Cancer

2016 ◽  
pp. 81-88 ◽  
Author(s):  
Martin Brown ◽  
Meiyun Fan
Keyword(s):  
Breast Cancer ◽  
Cultured Cells

scholarly journals Combined Luteolin and Indole-3-Carbinol Synergistically Constrains ERα-Positive Breast Cancer by Dual Inhibiting Estrogen Receptor Alpha and Cyclin-Dependent Kinase 4/6 Pathway in Cultured Cells and Xenograft Mice

Cancers ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2116
Author(s):  
Xiaoyong Wang ◽  
Lijuan Zhang ◽  
Qi Dai ◽  
Hongzong Si ◽  
Longyun Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Cultured Cells ◽  
Inhibitory Effect ◽  
Cyclin Dependent Kinase ◽  
Xenograft Mice ◽  
The Individual

The high concentrations of individual phytochemicals in vitro studies cannot be physiologically achieved in humans. Our solution for this concentration gap between in vitro and human studies is to combine two or more phytochemicals. We screened 12 phytochemicals by pairwise combining two compounds at a low level to select combinations exerting the synergistic inhibitory effect of breast cancer cell proliferation. A novel combination of luteolin at 30 μM (LUT30) and indole-3-carbinol 40 μM (I3C40) identified that this combination (L30I40) synergistically constrains ERα+ breast cancer cell (MCF7 and T47D) proliferation only, but not triple-negative breast cancer cells. At the same time, the individual LUT30 and I3C40 do not have this anti-proliferative effect in ERα+ breast cancer cells. Moreover, this combination L30I40 does not have toxicity on endothelial cells compared to the current commercial drugs. Similarly, the combination of LUT and I3C (LUT10 mg + I3C10 mg/kg/day) (IP injection) synergistically suppresses tumor growth in MCF7 cells-derived xenograft mice, but the individual LUT (10 mg/kg/day) and I3C (20 mg/kg/day) do not show an inhibitory effect. This combination synergistically downregulates two major therapeutic targets ERα and cyclin dependent kinase (CDK) 4/6/retinoblastoma (Rb) pathway, both in cultured cells and xenograft tumors. These results provide a solid foundation that a combination of LUT and I3C may be a practical approach to treat ERα+ breast cancer cells after clinical trials.

scholarly journals Synthesis and Biological Evaluation of New 3,4-diarylmaleimides as Enhancers (modulators) of Doxorubicin Cytotoxic Activity on Cultured Tumor Cells from a Real Case of Breast Cancer

2017 ◽  
Vol 61 (1) ◽  
Author(s):  
Jessica R. Gutierrez-Cano ◽  
Pradip D. Nahide ◽  
Velayudham Ramadoss ◽  
Yuvraj Satkar ◽  
Rafael Ortiz-Alvarado ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cultured Cells ◽  
Biological Evaluation ◽  
Doxorubicin Treatment ◽  
P Glycoprotein ◽  
Molecular Action ◽  
Mortality Effect ◽  
Kinase Phosphorylation ◽  
Synthesis And Biological Evaluation ◽  
Cultured Tumor Cells

<p>A series of new 3,4-diarylmaleimides were synthesized in an optimized and efficient lineal sequence of three steps, starting from commercial maleimide. The biological evaluation of these compounds as enhancers (activity modulators) in the co-administration with doxorubicin treatment in breast cancer cells directly obtained from a patient, were essayed. The cancerous tissue BT026-512N was provided by the National Institute of Cancerology (INCAN) of México. This tissue was obtained by biopsy from a patient diagnosed with stage IIB ductal breast cancer. The results obtained in the assays, show decreased cell viability on the cultured cells for all of the maleimides synthesized in combinatorial administration with doxorubicin. The highest mortality effect was determined for maleimides <strong>9</strong> and <strong>29</strong> increased in close to three times the effect compared with treatment using only doxorubicin. Based on previous functionalized maleimides core reports and Molinspiration chemoinformatic analysis, these results could possibly point out to the Pg-p glycoprotein as bio-molecular action target of maleimides by kinase phosphorylation-inhibition, although more experimental data is necessary.</p>

Breast Cancer Takes up 99mTc Bombesin. A Preliminary Report

2002 ◽  
Vol 88 (3) ◽  
pp. S25-S28 ◽  
Author(s):  
F Scopinaro ◽  
A Varvarigou ◽  
W Ussof ◽  
G De Vincentis ◽  
S Archimandritis ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Primary Breast Cancer ◽  
Cultured Cells ◽  
Metastatic Breast ◽  
Axillary Node ◽  
Lateral View ◽  
Lymph Node Staging ◽  
Breast Cancer Patients ◽  
Time Activity ◽  
Total Body

Background Several tumors including lung, prostate, ovarian, colon, and exocrine pancreatic cancer show receptors for the amphibian neurotransmitter and growth factor bombesin (BN) and its mammalian counterparts gastrin-releasing peptide and neuromedin B. Also breast cancer has been reported to show such receptors: the presence of BN receptors in primary breast cancer has been demonstrated on cultured cells and by autoradiography on breast tissue samples. Authors who have studied BN receptors in breast cancer do not agree on their frequency in primary cancer, but indicate that 100% of metastatic breast cancers show such receptors. Methods We examined three primary breast cancer patients with 99mTc BN and 99mTc sestamibi one week before surgery. One of them showed axillary node invasion. The same acquisition technique was used for breast and chest imaging with both radiopharmaceuticals, whereas total body images were acquired only with 99mTc BN. Also the administered radioactivity was different: 20 mCi of 99mTc sestamibi and 5-8 mCi of 99mTc BN. Dynamic images were acquired for 20 mins after iv injection with the patient in ventral decubitus and the gamma camera positioned in lateral view, as is generally done in Khakhali's prone scintimammography. Anterior chest images were acquired for 30 mins. Prone scintimammography was performed one hour after administration of both tracers. ROIs were drawn on tumors and surrounding breast with the same technique in order to calculate the tumor to breast ratio (T/B). In addition, total body scan was performed one hour and three hours after 99mTc BN administration. All three patients underwent breast conserving surgery with lymphadenectomy. Postoperative pathologic assessment showed the following T and N stages in the three patients: T1bN0, T1cN0. and T1cN1. Results All three cancers were imaged with both tracers. The T/B of 99mTc BN was always higher than that of 99mTc sestamibi. Chest uptake was always much higher with 99mTc sestamibi than with 99mTc BN. Comparison between 99mTc BN and 99mTc sestamibi images gave other intriguing results: in the N1 patient both tracers clearly imaged the invaded node, but on the 99mTc BN image the primary tumor was larger than on the 99mTc sestamibi image and the node was smaller. It is known that 99mTc BN is not taken up by vessels and inflammatory tissue. The time activity curves of the two tracers were significantly different in all patients, with an increase in 99mTc BN uptake in the first three to five minutes, followed by a less sharp uprise of the curve, quite similar to a plateau. Conclusions Our first impression is that 99mTc BN is a useful breast cancer seeking agent and very promising for lymph node staging.

scholarly journals Compressive stress-mediated p38 activation required for ERα + phenotype in breast cancer

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Pauliina M. Munne ◽  
Lahja Martikainen ◽  
Iiris Räty ◽  
Kia Bertula ◽  
Nonappa ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cultured Cells ◽  
Ex Vivo ◽  
Therapeutic Interventions ◽  
Preclinical Model ◽  
Matrix Stiffness ◽  
Breast Cancers ◽  
Ex Vivo Model ◽  
Major Barrier ◽  
The Matrix

AbstractBreast cancer is now globally the most frequent cancer and leading cause of women’s death. Two thirds of breast cancers express the luminal estrogen receptor-positive (ERα + ) phenotype that is initially responsive to antihormonal therapies, but drug resistance emerges. A major barrier to the understanding of the ERα-pathway biology and therapeutic discoveries is the restricted repertoire of luminal ERα + breast cancer models. The ERα + phenotype is not stable in cultured cells for reasons not fully understood. We examine 400 patient-derived breast epithelial and breast cancer explant cultures (PDECs) grown in various three-dimensional matrix scaffolds, finding that ERα is primarily regulated by the matrix stiffness. Matrix stiffness upregulates the ERα signaling via stress-mediated p38 activation and H3K27me3-mediated epigenetic regulation. The finding that the matrix stiffness is a central cue to the ERα phenotype reveals a mechanobiological component in breast tissue hormonal signaling and enables the development of novel therapeutic interventions. Subject terms: ER-positive (ER + ), breast cancer, ex vivo model, preclinical model, PDEC, stiffness, p38 SAPK.

scholarly journals New Trends for Antimalarial Drugs: Synergism between Antineoplastics and Antimalarials on Breast Cancer Cells

Biomolecules ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 1623
Author(s):  
Diana Duarte ◽  
Nuno Vale
Keyword(s):  
Breast Cancer ◽  
Cancer Therapy ◽  
Cell Viability ◽  
Cultured Cells ◽  
Fixed Ratio ◽  
Tumor Cell Line ◽  
New Combination ◽  
Breast Cancer Therapy ◽  
Almost All ◽  
Mcf 7

Chemotherapy plays a key role in breast cancer therapy, but drug resistance and unwanted side effects make the treatment less effective. We propose a new combination model that combines antineoplastic drugs and antimalarials for breast cancer therapy. Cytotoxic effects of two antineoplastic agents alone and in combination with several antimalarials on MCF-7 tumor cell line was evaluated. Different concentrations in a fixed ratio were added to the cultured cells and incubated for 48 h. Cell viability was evaluated using MTT and SRB assays. Synergism was evaluated using the Chou-Talalay method. The results indicate doxorubicin (DOX) and paclitaxel (PTX) alone at concentrations of their IC50 and higher are cell growth inhibitors. Mefloquine, artesunate, and chloroquine at concentrations of their IC50 demonstrate anti-cancer activity. In combination, almost all antimalarials demonstrate higher ability than DOX and PTX alone to decrease cell viability at concentrations of IC50 and lower than their IC50. The combination of chloroquine, artesunate and mefloquine with DOX and PTX was synergic (CI < 1). The combination of DOX and mefloquine after 48 h incubation demonstrated the highest cytotoxicity against MCF-7 cells, and the combination of DOX and artesunate was the most synergic. These results suggest antimalarials could act synergistically with DOX/PTX for breast cancer therapy.

scholarly journals Human Hydroxysteroid (17-β) Dehydrogenase 1 Expression Enhances Estrogen Sensitivity of MCF-7 Breast Cancer Cell Xenografts

Endocrinology ◽  
2006 ◽  
Vol 147 (11) ◽  
pp. 5333-5339 ◽  
Author(s):  
Bettina Husen ◽  
Kaisa Huhtinen ◽  
Taija Saloniemi ◽  
Josef Messinger ◽  
Hubert H. Thole ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cultured Cells ◽  
Human Breast ◽  
Expression Plasmid ◽  
Estrogen Sensitivity ◽  
Uterine Growth ◽  
Dependent Growth ◽  
Mcf 7

Hydroxysteroid (17-β) dehydrogenase 1 (HSD17B1) catalyzes the conversion between estrone (E1) and estradiol (E2). The reaction is reversible in vitro, but the data in cultured cells suggest that E2 production is the predominant reaction in physiological conditions. However, the hypothesis has not been verified in vivo. In the present study, estrogen-dependent MCF-7 human breast cancer cells were stably transfected with an expression plasmid for human HSD17B1. The enzyme efficiently converted E1 to E2 and enhanced the estrogen-dependent growth of cultured MCF-7 cells in the presence of hormonally less active E1. The HSD17B1-expressing cells also formed estrogen-dependent tumors in immunodeficient nude mice. After treating the mice with an appropriate dose of the substrate (E1, 0.1 μmol/kg·d), a marked difference in tumor growth was observed between nontransfected and HSD17B1-transfected MCF-7 cells, mean tumor weights at the end of E1 treatment being 23.2 and 130.4 mg, respectively. Furthermore, estrogen-dependent growth of the HSD17B1-expressing xenografts in the presence of E1 was markedly inhibited by administering 5 μmol/kg·d of a specific HSD17B1 inhibitor. After a 4-wk treatment, the tumor size was reduced by 59.8% as compared with the nontreated tumors, whereas the uterine growth of the mice was not affected by the HSD17B1 inhibitor used. This was in line with the induction of apoptosis of the tumors. The results evidently show that estrogenic response for E1 is enhanced by the local action of HSD17B1 in vivo, and thus, the enzyme is a potential target for pharmacological inhibition of estrogen action.

scholarly journals The effect of Euphorbia szovitsii Fisch. & C.A.Mey extract on the viability and the proliferation of MDA-MB-231 cell line

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Majid Asadi-Samani ◽  
Mahmoud Rafieian-Kopaei ◽  
Zahra Lorigooini ◽  
Hedayatollah Shirzad
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Cell Line ◽  
Cultured Cells ◽  
Cancer Cell Line ◽  
Annexin V ◽  
Underlying Mechanism ◽  
Dependent Manner ◽  
Cycle Arrest

Abstract Some medicinal herbs and compounds are known to target cancer cells, but the success of them as anticancer compounds depends to a large extent on their ability to activate pathways that kill cancer cells by arresting cell cycle and inducing apoptosis. The aim of the present study was to determine the anticancer effects of Euphorbia szovitsii Fisch. & C.A.Mey. on the breast cancer cells to reveal the underlying mechanism of its anti-breast cancer properties. In this experimental study, triple negative breast cancer cell line (MDA-MB-231) was cultivated in RPMI-1640 medium. Hydroalcoholic extract (70:30) of aerial parts of the plant was prepared. The cultured cells were treated with different concentrations (0–1000 μg/ml) of E. szovitsii extract for 24 and 48 h. Toxicity of the extract on MDA-MB-231 cells was examined using MTT (3-[4,5-dimethyl-2-thiazolyl]-2, 5 diphenyl tetrazolium bromide) test. The Annexin V–FITC Apoptosis Detection Kit was used to evaluate apoptosis and necrosis. Flow cytometry technique was employed to differentiate different phases of the cell cycle in the cells. Data were analyzed by GraphPad Prism and SPSS software. After 24 and 48 h, the IC50 values were respectively 76.78 (95% CI = 60.75–97.05; R = 0.8588) and 59.71 (95% CI = 46.25–77.09; R = 0.8543) μg/ml for E. szovitsii. The extract exhibited antiproliferative effects against MDA-MB-231 cells in a dose-dependent manner. Annexin V-FITC/PI assay confirmed that the extract was able to induce apoptosis in MDA-MB-231 cells. Moreover, treatment with the extract resulted in cell cycle arrest at G1 phase. Therefore, E. szovitsii could induce apoptosis and cycle arrest in the MDA-MB-231 cell line. It might be a good resource of natural products for producing anti-breast cancer drugs.

Oestradiol is effective in stimulating3H-Thymidine Incorporation But Not On Proliferation of Breast Cancer Cultured Cells

1985 ◽  
Vol 18 (4) ◽  
pp. 457-464
Author(s):  
S. Jozan ◽  
G. Gay ◽  
B. Marques ◽  
A. Mirouze ◽  
J. F. David
Keyword(s):  
Breast Cancer ◽  
Cultured Cells ◽  
Thymidine Incorporation

scholarly journals Small-Molecule “BRCA1-Mimetics” Are Antagonists of Estrogen Receptor-α

2014 ◽  
Vol 28 (12) ◽  
pp. 1971-1986 ◽  
Author(s):  
Yongxian Ma ◽  
York Tomita ◽  
Anju Preet ◽  
Robert Clarke ◽  
Erikah Englund ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Small Molecule ◽  
Cultured Cells ◽  
Binding Pocket ◽  
Estrogen Receptor Α ◽  
Estrogen Receptor Modulators ◽  
Binding Interface ◽  
Ic50 Values ◽  
Α Activity

Context: Resistance to conventional antiestrogens is a major cause of treatment failure and, ultimately, death in breast cancer. Objective: The objective of the study was to identify small-molecule estrogen receptor (ER)-α antagonists that work differently from tamoxifen and other selective estrogen receptor modulators. Design: Based on in silico screening of a pharmacophore database using a computed model of the BRCA1-ER-α complex (with ER-α liganded to 17β-estradiol), we identified a candidate group of small-molecule compounds predicted to bind to a BRCA1-binding interface separate from the ligand-binding pocket and the coactivator binding site of ER-α. Among 40 candidate compounds, six inhibited estradiol-stimulated ER-α activity by at least 50% in breast carcinoma cells, with IC50 values ranging between 3 and 50 μM. These ER-α inhibitory compounds were further studied by molecular and cell biological techniques. Results: The compounds strongly inhibited ER-α activity at concentrations that yielded little or no nonspecific toxicity, but they produced only a modest inhibition of progesterone receptor activity. Importantly, the compounds blocked proliferation and inhibited ER-α activity about equally well in antiestrogen-sensitive and antiestrogen-resistant breast cancer cells. Representative compounds disrupted the interaction of BRCA1 and ER-α in the cultured cells and blocked the interaction of ER-α with the estrogen response element. However, the compounds had no effect on the total cellular ER-α levels. Conclusions: These findings suggest that we have identified a new class of ER-α antagonists that work differently from conventional antiestrogens (eg, tamoxifen and fulvestrant).

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