Inhibition of cell growth and telomerase activity of breast cancer cells in vitro by retinoic acids.

2000 ◽  
Author(s):  
S H Choi ◽  
H K Kang ◽  
E O Im ◽  
Y J Kim ◽  
Y T Bae ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Telomerase Activity ◽  
Retinoic Acids

PEAK1 promotes invasion and metastasis and confers drug resistance in breast cancer

2021 ◽  
Author(s):  
xingang wang ◽  
YAN ZHENG ◽  
YU WANG
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Cell Growth ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Multi Drug Resistance ◽  
Cancer Tissues

Abstract Background and AimsPseudopodium-enriched atypical kinase 1 (PEAK1) has reported to be upregulated in human malignancies and related with poor prognosis. Enhanced PEAK1 expression facilitates tumor cell survival, invasion, metastasis and chemoresistance. However, the role of PEAK1 in breast cancer is not clear. Here, we investigated the PEAK1 expression in breast cancer and analyzed its relation with clinicopathological status and chemotherapy resistance to the neoadjuvant chemotherapy (NAC). We also investigated the role of PEAK1 on breast cancer cells in vitro and in vivo. MethodsImmunohistochemistry (IHC) was performed in 112 surgical resected breast cancer tissues. The associations between clinicopathological status, multi-drug resistance and PEAK1 expression were determined. Effect of PEAK1 overexpression or down-expression on proliferation, colony formation, invasion, migration, metastasis and Doxorubicin sensitivity in the MCF-7 cells in vitro and in vivo was detected. ResultsPEAK1 was overexpressed in breast cancer tissues and NAC -resistant breast cancer tissues. High PEAK1 expression was related with tumor size, high tumor grade, T stage, LN metastasis, recurrence, Ki-67 expression, Her-2 expression and multi-drug resistance. Targeting PEAK1 inhibited cell growth, invasion, metastasis and reversed chemoresistance to Doxorubicin in breast cancer cells in vitro and in vivo. ConclusionHigh PEAK1 expression was associated with invasion, metastasis and chemoresistance of breast cancers. Furthermore, targeting PEAK1 could inhibit cell growth and metastasis, and reverse chemoresistance in breast cancer cells, which provides an effective treatment strategies for breast cancer.

scholarly journals Preparation of optimized lipid-coated calcium phosphate nanoparticles for enhanced in vitro gene delivery to breast cancer cells

2015 ◽  
Vol 3 (33) ◽  
pp. 6805-6812 ◽  
Author(s):  
Jie Tang ◽  
Li Li ◽  
Christopher B. Howard ◽  
Stephen M. Mahler ◽  
Leaf Huang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Calcium Phosphate ◽  
Cell Growth ◽  
Gene Delivery ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cancer Cell Growth ◽  
Calcium Phosphate Nanoparticles ◽  
Transfection Agent

The optimized lipid coated calcium phosphate nanoparticles more efficiently deliver functional siRNA and inhibit the cancer cell growth, in comparison with the commercial transfection agent OligofactamineTM.

scholarly journals PEAK1 promotes invasion and metastasis and confers drug resistance in breast cancer

2021 ◽  
Author(s):  
Xingang Wang ◽  
Yan Zheng ◽  
Yu Wang
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Chemotherapy Resistance ◽  
Ki 67 ◽  
Cancer Tissues

AbstractPseudopodium-enriched atypical kinase 1 (PEAK1) has been reported to be upregulated in human malignancies and is correlated with a poor prognosis. Enhanced PEAK1 expression facilitates tumor cell survival, invasion, metastasis and chemoresistance. However, the role of PEAK1 in breast cancer is unclear. We investigated PEAK1 expression in breast cancer and analyzed the relationship with clinicopathological status and chemotherapy resistance. We also investigated the role of PEAK1 in breast cancer cells in vitro and in vivo. Immunohistochemistry for PEAK1 was performed in 112 surgically resected breast cancer tissues. The association between clinicopathological status, chemotherapy resistance and PEAK1 expression was determined. The effect of PEAK1 overexpression or downregulation on proliferation, colony formation, invasion, migration, metastasis and doxorubicin sensitivity in MCF-7 cells in vitro and in vivo was studied. PEAK1 was overexpressed in breast cancer tissues. High PEAK1 expression was correlated with tumor size, high tumor grade, tumor stage, lymph node metastasis, recurrence, Ki-67 expression, Her-2 expression and chemotherapy resistance. Inhibiting PEAK1 decreased cell growth, invasion, metastasis and reversed chemoresistance to doxorubicin in breast cancer cells both in vitro and in vivo. High PEAK1 expression was associated with the invasion, metastasis and chemoresistance of breast cancers. Furthermore, targeting PEAK1 inhibited cell growth and metastasis and reversed chemoresistance in breast cancer cells. Targeting PEAK1 could be an effective treatment strategy for breast cancer.

scholarly journals Resveratrol down-regulates the growth and telomerase activity of breast cancer cells in vitro

2006 ◽  
Author(s):  
Giulia Lanzilli ◽  
Maria Fuggetta ◽  
Maria Tricarico ◽  
Andrea Cottarelli ◽  
Annalucia Serafino ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Telomerase Activity

IN-VITRO AND IN-VIVO STUDIES OF THE POSSIBLE CHEMOPREVENTIVE FUNCTIONS OF SOYBEAN ISOFLAVONE AND FLAVONOIDS ON BREAST CANCER

2019 ◽  
Vol 31 (06) ◽  
pp. 1950045
Author(s):  
Shoei-Loong Lin ◽  
Ming-Tse Lin ◽  
Mei-Yan Chen ◽  
Ting-Kai Leung
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Cell Growth ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
In Vivo Experiment ◽  
Mcf 7

Objectives: In this study, we assess the possible influence of soybean isoflavone (genistein) and other flavonoids (quercetin and catechin) on breast cancer chemoprevention. We design in-vitro and in-vivo experiments to analyze the effect of genistein, quercetin and catechin on cell proliferation, cell migration, and angiogenesis of breast cancer cells. Methods: In cell proliferation experiment, MCF-7 cells, SKBR-3 cells, and HUVEC cells were treated with genistein and other flavonoids (catechin and/or quercetin) for 48[Formula: see text]h to assess the influence on cell growth of normal and breast cancer cells. In cell motility test, we analyze the effect of isoflavone and flavonoids on migration ability of MCF-7 cells by 16[Formula: see text]h and SKBR-3 cells by 24[Formula: see text]h in two different concentrations (1.25[Formula: see text][Formula: see text]g/ml and 2.5[Formula: see text][Formula: see text]g/ml). In the in-vivo experiment, SKBR-3 cells mixed with PBS and catechin, respectively, were injected subcutaneously into nude mice, then we investigated the effect of catechin on cell growth by observing subcutaneous tumor size changes after 15 days. Results: The results suggest that genistein and quercetin can significantly inhibit proliferation of breast cancer cells, and their inhibitory effects are independent of estrogen receptor. In cell motility tests, all of the three phytochemicals were effective in the inhibition of cell migration on two breast cancer cell lines, except for quercetin on cell migration of SKBR-3 cell line. In the in-vitro experiment, catechin showed stimulatory effect on cell proliferation of HUVEC cell line, which may consider positive effect on angiogenesis, rather than inhibitory effect. However, in the in-vivo experiment, it showed no significant change in tumor size between the groups of with and without catechin treatment. Conclusions: According to our study, the results suggest that isoflavone and flavonoids tend to inhibit cell growth and metastasis of breast cancer cells. Our in-vivo experiment does not reach a significant result, and it may be due to lower catechin concentration. Under in-vivo environment, we should also consider the possible metabolic forms of catechin that cause different result from the in-vitro study.

scholarly journals Upregulation of SHMT2 Promotes Tumor Growth and Poor Prognosis of Breast Cancer through Activating VEGF and MAPK Signaling Pathway

2021 ◽  
Author(s):  
Shuang-Yan Xie ◽  
Dingbo Shi ◽  
Fei Lin ◽  
Xiao-Yu Cheng ◽  
Tong-chao Cheng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
Mapk Signaling ◽  
Nucleotide Metabolism ◽  
Breast Cancers ◽  
Apoptosis Pathway

Abstract Background: Serine hydroxymethyltransferase 2 (SHMT2) is a key enzyme in Serine/glycine metabolism. SHMT2 is very important for tumor cell growth and proliferation as well as metabolism. Here, we investigated the regulatory effects of SHMT2 on breast cancers growth and identified the underlying mechanisms of functions.Methods: We detected the expression of SHMT2 in breast cancer cells and tissues by immunohistochemistry and Western blotting.We investigated the functional and molecular mechanisms by which SHMT2 downregulation or overexpression regulates the growth and apoptosis of breast cancer cells in vivo and in vitro. Results: We found SHMT2 was highly expressed in BRCA cell lines and tumor tissues. Strong SHMT2 expression showed a positive correlation with the poor prognoses of patients with breast cancers. SHMT2 knockdown by shRNA significantly inhibited cell growth and induced apoptosis in vitro, and whereas SHMT2 overexpression promoted tumor growthin in subcutaneous xenograft model. RNA-seq revealed that high expression of SHMT2 not only promoted serine metabolism, nucleotide metabolism, oxidative phosphorylation and proteasome independent degradation pathways. It also activated the cell survival signaling pathway and antagonized the apoptosis pathway. The observed molecular regulation of cell growth was accompanied by the activited of the MAPK, VEGF pathways and suppressed of the mitochondrial mediated apoptosis pathway that was mediated by the SHMT2 up-regulation. Conclusions: These results indicate that SHMT2 plays a critical role in regulating breast cancers growth and could serve as a therapeutic target for breast cancer therapy.

N-hexane Extract and Fraction of Green Tea as Antiproliferation of MCM-B2 Breast Cancer Cells In Vitro

2020 ◽  
Vol 6 (2) ◽  
Author(s):  
Lisni Noraida Waruwu ◽  
Maria Bintang ◽  
Bambang Pontjo Priosoeryanto
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Green Tea ◽  
Cancer Cell ◽  
Breast Cancer Cells ◽  
Green Tea Extract ◽  
Hexane Fraction ◽  
Phytochemical Screening ◽  
Tea Extract

Green tea (Camellia sinensis) is one of traditional plants that have the potential as an anticancer. The sample used in this research commercial green tea extract. The purpose of this study was to test the antiproliferation activity of green tea extract on breast cancer cell MCM-B2 in vitro. Green tea extract fractionated using three solvents, ie water, ethanol 70%, and n-hexane. Extract and fraction of green tea water have value Lethality Concentration 50 (LC50) more than 1000 ppm. The fraction of ethanol 70% and n-hexane had an LC50 value of 883.48 ppm and 600.56 ppm, respectively. The results of the phytochemical screening of green tea extract are flavonoids, tannins, and saponins, while the phytochemical screening results of n-hexane fraction are flavonoids and tannins. Antiproliferation activity was tested on breast cancer cells MCM-B2 and normal cells Vero by trypan blue staining method. The highest MCM-B2 cell inhibitory activity was achieved at a concentration of 13000 ppm green tea extract and 1000 ppm of n-hexane fraction, 59% and 59%, respectively. The extract and n-hexane fraction of green tea are not toxic to normal Vero cells characterized by not inhibiting normal cell proliferation. Keywords: antiproliferative, cancer cell MCM-B2, commercial green tea, cytotoxicity

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