scholarly journals MARCADORES TUMORALES PRONÓSTICOS EN CÁNCER DE MAMA: BAX y Bcl-2

2022 ◽  
Vol 7 (1) ◽  
pp. 24
Author(s):  
Lizette Elena Leiva Suero ◽  
Yenddy Carrero Castillo ◽  
Graciela de las Mercedes Quishpe Jara ◽  
Sandra Villacís Valencia ◽  
Jesús Onorato Chicaiza Tayupanta ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Carcinoma ◽  
Tumor Markers ◽  
Inhibitory Effect ◽  
Cáncer De Mama ◽  
Cell Models ◽  
Culture Cells ◽  
Carcinoma De Mama ◽  
Marcadores Tumorales ◽  
Mcf 7

Introducción: El carcinoma de mama representa el 16% de todos los cánceres femeninos, cada año en las Américas, más de 462,000 mujeres son diagnosticadas y casi 100,000 mueren por esta causa, por lo que la detección de nuevos marcadores pronósticos se hace imprescindible para el desarrollo de nuevas terapias oncológicas. Objetivo: Identificar los marcadores tumorales con fines pronósticos en cáncer de mama en células de cultivo de carcinoma de mama MCF7. Método: Se desarrolló un estudio explicativo longitudinal y prospectivo observacional para identificar marcadores tumorales con valor pronóstico en modelos celulares MCF7 de Cáncer de Mama, se utilizarán métodos estadísticos descriptivos e inferenciales. Resultados: Se identificó un predominio de Bcl-2 en las células de cultivo MCF7 de Carcinoma de Mama. Conclusión: La identificación de BAX y Bcl-2 en modelos celulares MCF 7 de Carcinoma de Mama permite evaluar nuevas opciones terapéuticas relacionadas con la inducción de la apoptosis. La predominancia Bcl-2 pudiera constituir un factor de mal pronóstico y menor supervivencia debido a su efecto inhibidor de la apoptosis, donde subyacen alteraciones mitocondriales, que inciden en la regulación del nivel de calcio intracelular, o por su efecto antioxidante.   Palabras clave: Neoplasias de la mama, Pronóstico, Apoptosis, Proteína de Susceptibilidad a Apoptosis Celular   ABSTRACT    Introduction: Breast carcinoma represents 16% of all female cancers, each year in the Americas, more than 462,000 women are diagnosed and almost 100,000 die from this cause, so the detection of new prognostic markers is essential for the development of new oncological therapies. Objective: To identify tumor markers for prognostic purposes in breast cancer in MCF7 breast carcinoma culture cells. Method: A longitudinal and prospective observational explanatory study was developed to identify tumor markers with prognostic value in MCF7 cell models of Breast Cancer, descriptive and inferential statistical methods will be used. Results: A predominance of Bcl-2 was identified in the MCF7 culture cells of Breast Carcinoma. Conclusion: The identification of BAX and Bcl-2 in MCF 7 cell models of Breast Carcinoma allows to evaluate new therapeutic options related to the induction of apoptosis. The Predominance bcl-2 could constitute a factor of poor prognosis and lower survival due to its inhibitory effect of apoptosis, where mitochondrial alterations underlie, which affect the regulation of the level of intracellular calcium, or for its antioxidant effect. Keywords: Breast Neoplasms, Prognosis, Apoptosis, Cellular Apoptosis Susceptibility Protein

Intronic miRNAs of Apoptosis Genes as Indicators of Cell Death

2019 ◽  
Vol 35 (6) ◽  
pp. 108-113
Author(s):  
J.A. Makarova ◽  
A.A. Poloznikov
Keyword(s):  
Breast Cancer ◽  
Cancer Cell Line ◽  
Ministry Of Education ◽  
Apoptosis Induction ◽  
Cell Models ◽  
Process Stage ◽  
Mature Micrornas ◽  
The Russian Federation ◽  
Apoptosis Level ◽  
Mcf 7

A method to assess the apoptosis level in cell models based on the analysis of the expression of micRNAs located in introns of apoptosis genes has been developed. Bioinformation analysis identified 536 genes associated with apoptosis; 30 of them contained 38 pre-microRNAs encoding 41 mature microRNAs. A significant change in the expression of hsa-miR-1244 and hsa-miR-4479 in response to apoptosis induction in the MCF-7 breast cancer cell line was revealed. A correlation was also found between the expression level of these miRNAs and the size of the primary tumor (process stage) in patients with breast cancer. apoptosis, microRNA, MCF7, breast cancer This work was supported by the Ministry of Education and Science of the Russian Federation (Project no. RFMEFI61618X0092).

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.

Effects of Simvastatin on Breast Carcinoma Cell Proliferation and Apoptosis via Transforming Growth Factor-β1/Smad3 Pathway

2021 ◽  
Vol 11 (9) ◽  
pp. 1673-1682
Author(s):  
Feng Wang ◽  
Gengbao Qu ◽  
Baokai Wang
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Breast Carcinoma ◽  
Protein Expression ◽  
Breast Cancer Cell ◽  
Cell Apoptosis ◽  
Carcinoma Cell ◽  
Proliferation And Apoptosis ◽  
Smad3 Protein ◽  
Mcf 7

Objective: To investigate the function and causative role of simvastatin (Sim) in breast carcinoma cell apoptosis as well as proliferation. Methods: 20 breast carcinoma patients requiring surgery were treated with Sim (20 days, 30 mg), and samples of pre-treatment (pre) and post-treatment (post) were acquired. We detected tissue cell proliferation and apoptosis changes and used functional experiments to detect cell proliferation and apoptosis changes after treating not only estrogen receptor (ER)-positive (MCF-7) but also ER-negative cells (MDA-MB-231) with Sim or TGF-β1. Detection of p-Smad3 and total Smad3 protein expression changes was conducted, and we finally used in vivo experiments to assess the influence of Sim on breast tumor growth and drug safety. Results: Immunohistochemistry and TUNEL staining results showed that after treatment with Sim, breast carcinoma cell proliferation decreased and apoptosis increased. Functional experiments results showed that Sim notedly promoted the MDA-MB-231 and MCF-7 cell apoptosis, inhibiting migration, proliferation and epithelial mesenchymal transition. Moreover, TGF-β1 protein expression was strikingly lower in Sim group than that in DMSO group. When TGF-β1 and Sim were combined to use, the inhibitory ability of Sim on breast cancer cell proliferation markedly increased and the capability of TGF-β1 protein inducing p-Smad3 protein increased. In addition, after Sim treatment in mice, the tumor volume became smaller, the pathological changes weakened, and there was no significant effect on liver function and kidney function. Conclusion: Sim participates in breast cancer cell apoptosis and proliferation via regulating TGF-β1/Smad3 signal pathway.

scholarly journals TRAIL-Induced Apoptosis in TRAIL-Resistant Breast Carcinoma Through Quercetin Cotreatment

2018 ◽  
Vol 12 ◽  
pp. 117822341774985 ◽  
Author(s):  
Jasmine M Manouchehri ◽  
Katherine A Turner ◽  
Michael Kalafatis
Keyword(s):  
Breast Cancer ◽  
Breast Carcinoma ◽  
Human Tumor ◽  
Breast Cancers ◽  
Treatment Regimens ◽  
Efficacious Treatment ◽  
Induced Apoptosis ◽  
Necrosis Factor ◽  
Mcf 7

Breast cancer is the most commonly diagnosed cancer in women. There is a continued interest for the development of more efficacious treatment regimens for breast carcinoma. Recombinant human tumor necrosis factor–related apoptosis-inducing ligand (rhTRAIL) shows potential as a potent anticancer therapeutic for the treatment of breast cancer, whereas displaying minimal toxicity to normal cells. However, the promise of rhTRAIL for the treatment of breast cancer is dismissed by the resistance to rhTRAIL-induced apoptosis exhibited by many breast cancers. Thus, a cotreatment strategy was examined by applying the natural compound quercetin (Q) as a sensitizing agent for rhTRAIL-resistant breast cancer BT-20 and MCF-7 cells. Quercetin was able to sensitize rhTRAIL-resistant breast cancers to rhTRAIL-induced apoptosis as detected by Western blotting through the proteasome-mediated degradation of c-FLIPL and through the upregulation of DR5 expression transcriptionally. Overall, these in vitro findings establish that Q is an effective sensitizing agent for rhTRAIL-resistant breast cancers.

scholarly journals Studies on Multifunctional Effect of All-Trans Retinoic Acid (ATRA) on Matrix Metalloproteinase-2 (MMP-2) and Its Regulatory Molecules in Human Breast Cancer Cells (MCF-7)

2009 ◽  
Vol 2009 ◽  
pp. 1-13 ◽  
Author(s):  
Anindita Dutta ◽  
Triparna Sen ◽  
Aniruddha Banerji ◽  
Shamik Das ◽  
Amitava Chatterjee
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Gelatin Zymography ◽  
Inhibitory Effect ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Atra Treatment ◽  
Mcf 7

Background. Vitamin A derivative all-trans retinoic acid (ATRA) is considered as a potent chemotherapeutic drug for its capability of regulating cell growth and differentiation. We studied the effect of ATRA on MMP-2 in MCF-7, human breast cancer cells, and the probable signaling pathways which are affected by ATRA on regulating pro-MMP-2 activity and expression.Methods. Gelatin zymography, RT-PCR, ELISA, Western blot, Immunoprecipitation, and Cell adhesion assay are used.Results. Gelatin zymography showed that ATRA caused a dose-dependent inhibition of pro-MMP-2 activity. ATRA treatment downregulates the expression of MT1-MMP, EMMPRIN, FAK, NF-kB, and p-ERK. However, expression of E-cadherin, RAR, and CRABP increased upon ATRA treatment. Binding of cells to extra cellular matrix (ECM) protein fibronectin reduced significantly after ATRA treatment.Conclusions. The experimental findings clearly showed the inhibition of MMP-2 activity upon ATRA treatment. This inhibitory effect of ATRA on MMP-2 activity in human breast cancer cells (MCF-7) may result due to its inhibitory effect on MT1-MMP, EMMPRIN, and upregulation of TIMP-2. This study is focused on the effect of ATRA on MMP, MMP-integrin-E-cadherin interrelationship, and also the effect of the drug on different signaling molecules which may involve in the progression of malignant tumor development.

scholarly journals Overexpression of wild-type p53 gene renders MCF-7 breast cancer cells more sensitive to the antiproliferative effect of progesterone

2003 ◽  
Vol 179 (1) ◽  
pp. 55-62 ◽  
Author(s):  
M Alkhalaf ◽  
AM El-Mowafy
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
P53 Protein ◽  
P53 Gene ◽  
Inhibitory Effect ◽  
Antiproliferative Effect ◽  
Mcf 7

We have recently shown that growth inhibition of breast cancer cells by progesterone is due to the induction of cell differentiation, but not apoptosis. Because the tumor suppressor protein p53 plays a central role in normal cell growth and in tumor suppression, we have examined the effect of progesterone on the levels of this protein in MCF-7 cells. We show here that the antiproliferative effect of progesterone is accompanied with down-regulation of endogenous p53 protein. To study the effect of progesterone on cell growth in the presence of normal levels of p53 protein, we used transient transfection to overexpress p53 protein. MCF-7 cells were transfected with a p53 expressing vector that contains p53 human cDNA under the control of a cytomegalovirus promoter. Cell growth, cell viability, and apoptosis were analyzed in the transfected cells after six days of exposure to 100 nM progesterone. We show here that progesterone significantly enhances growth inhibition and apoptosis in MCF-7 cells overexpressing p53, but not in cells transfected with the control vector. These data suggest that re-establishing p53 function in MCF-7 breast cancer cells renders them more sensitive to the growth inhibitory effect of progesterone.

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