scholarly journals DNA damage uncouples the mitogenic response to IGF-I in MCF-7 malignant breast cancer cells by switching the roles of PI3 kinase and p21WAF1/Cip1

2005 ◽  
Vol 116 (4) ◽  
pp. 506-513 ◽  
Author(s):  
Martin A. Clark ◽  
Claire M. Perks ◽  
Zoë E. Winters ◽  
Jeff M.P. Holly
Keyword(s):  
Breast Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Pi3 Kinase ◽  
Mitogenic Response ◽  
Igf I ◽  
Malignant Breast ◽  
Mcf 7

The secretome of non-tumorigenic mammary cells MCF-10A elicits DNA damage in MCF-7 and MDA-MB-231 breast cancer cells

2021 ◽  
Vol 70 ◽  
pp. 105018
Author(s):  
Guadalupe M. Vedoya ◽  
Marcela M. López Nigro ◽  
Gabriela A. Martín
Keyword(s):  
Breast Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Mammary Cells ◽  
Mcf 7

scholarly journals Induction of multidrug resistance associated protein 2 in tamoxifen-resistant breast cancer cells

2007 ◽  
Vol 14 (2) ◽  
pp. 293-303 ◽  
Author(s):  
Hoo Kyun Choi ◽  
Jin Won Yang ◽  
Sang Hee Roh ◽  
Chang Yeob Han ◽  
Keon Wook Kang
Keyword(s):  
Breast Cancer ◽  
Multidrug Resistance ◽  
Cancer Cells ◽  
Transcriptional Activation ◽  
Breast Cancer Cells ◽  
Pregnane X Receptor ◽  
Pi3 Kinase ◽  
Gene Promoters ◽  
Breast Cancer Patients ◽  
Mcf 7

Acquired resistance to tamoxifen (TAM) is a serious therapeutic problem in breast cancer patients. The transition from chemotherapy-responsive breast cancer cells to chemotherapy-resistant cancer cells is mainly accompanied by the increased expression of multidrug resistance-associated proteins (MRPs). In this study, it was found that TAM-resistant MCF-7 (TAMR-MCF-7) cells expressed higher levels of MRP2 than control MCF-7 cells. Molecular analyses using MRP2 gene promoters supported the involvement of the pregnane X receptor (PXR) in MRP2 overexpression in TAMR-MCF-7 cells. Although CCAAT/enhancer-binding protein β was overexpressed continuously in TAMR-MCF-7 cells, this might not be responsible for the transcriptional activation of the MRP2 gene. In addition, the basal activities of phosphatidylinositol 3-kinase (PI3-kinase) were higher in the TAMR-MCF-7 cells than in the control cells. The inhibition of PI3-kinase significantly reduced both the PXR activity and MRP2 expression in TAMR-MCF-7 cells. Overall, MRP2 induction plays a role in the additional acquisition of chemotherapy resistance in TAM-resistant breast cancer.

Processing of clustered DNA damage in human breast cancer cells MCF-7 with partial DNA-PKcs deficiency

2008 ◽  
Vol 269 (1) ◽  
pp. 174-183 ◽  
Author(s):  
Prakash Peddi ◽  
Dave C. Francisco ◽  
Angela M. Cecil ◽  
Jessica M. Hair ◽  
Mihalis I. Panayiotidis ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Clustered Dna Damage ◽  
Mcf 7

Cytotoxicity and DNA damage associated with pyrazoloacridine in MCF-7 breast cancer cells

1996 ◽  
Vol 51 (12) ◽  
pp. 1649-1659 ◽  
Author(s):  
Jean L. Grem ◽  
Pedro M. Politi ◽  
Stacey L. Berg ◽  
Nabil M. Benchekroun ◽  
Mahendra Patel ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Mcf 7

scholarly journals lncMat2B regulated by severe hypoxia induces cisplatin resistance by increasing DNA damage repair and tumor-initiating population in breast cancer cells

2020 ◽  
Vol 41 (11) ◽  
pp. 1485-1497 ◽  
Author(s):  
Alfredo García-Venzor ◽  
Edna Ayerim Mandujano-Tinoco ◽  
Araceli Ruiz-Silvestre ◽  
José Manuel Sánchez ◽  
Floria Lizarraga ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Ectopic Expression ◽  
Three Dimensional ◽  
Severe Hypoxia ◽  
Loss Of Function ◽  
Mcf 7

Abstract Multicellular tumor spheroids (MCTSs) constitute a three-dimensional culture system that recapitulates the in vivo tumor microenvironment. Tumor cells cultured as MCTSs present antineoplastic resistance due to the effect of microenvironmental signals acting upon them. In this work, we evaluated the biological function of a new microenvironment-regulated long non-coding RNA, lncMat2B, in breast cancer. In MCTSs, the expression of lncMat2B presented an increase and a zonal heterogeneity, as it was expressed principally in quiescent cells of hypoxic regions of the MCTSs. As expected, functional assays supported the role of severe hypoxia in the regulation of lncMat2B. Moreover, gain- and loss-of-function assays using a transcriptional silencing CRISPR/Cas9 system and gBlock revealed that lncMAT2B regulates the tumor-initiating phenotype. Interestingly, lncMat2B is overexpressed in a cisplatin-resistant MCF-7 cell line, and its ectopic expression in wild type MCF-7 cells increased survival to cisplatin exposure by reducing DNA damage and reactive oxygen species accumulation. lncMAT2B is a possible link between severe hypoxia, tumor-initiating phenotype and drug resistance in breast cancer cells.

scholarly journals The WT1 Wilms’ tumor suppressor gene product interacts with estrogen receptor-α and regulates IGF-I receptor gene transcription in breast cancer cells

2005 ◽  
Vol 35 (1) ◽  
pp. 135-144 ◽  
Author(s):  
Naama Reizner ◽  
Sharon Maor ◽  
Rive Sarfstein ◽  
Shirley Abramovitch ◽  
Wade V Welshons ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Gene Transcription ◽  
Breast Cancer Cells ◽  
Promoter Activity ◽  
Wilms Tumor ◽  
Estrogen Receptor Α ◽  
Igf I ◽  
Mcf 7

The IGF-I receptor (IGF-IR) has an important role in breast cancer development and progression. Previous studies have suggested that the IGF-IR gene is negatively regulated by a number of transcription factors with tumor suppressor activity, including the Wilms’ tumor protein WT1. The present study was aimed at evaluating the hypothesis that IGF-IR gene transcription in breast cancer cells is under inhibitory control by WT1 and, furthermore, that the mechanism of action of WT1 involves functional and physical interactions with estrogen receptor-α (ERα). Results of transient coexpression experiments showed that all four predominant isoforms of WT1 (including or lacking alternatively spliced exons 5 and 9) repressed IGF-IR promoter activity by 39–49%. To examine the potential interplay between WT1 and ERα in control of IGF-IR gene transcription we employed ER-depleted C4 cells that were generated by clonal selection of ER-positive MCF-7 cells that were maintained in estrogen-free conditions. IGF-IR levels in C4 cells were ~43% of the values in MCF-7 cells whereas WT1 levels in C4 cells were 4.25-fold higher than in MCF-7. Triple cotransfection experiments using an ERα expression vector in the absence or presence of WT1 expression vectors, along with an IGF-IR promoter reporter plasmid, revealed that ERα stimulated IGF-IR promoter activity whereas coexpression of WT1 abrogated the effect of ERα. In addition, co-immunoprecipitation experiments demonstrated a specific association between WT1 and ERα. Combined, our results suggest that WT1 suppresses IGF-IR gene transcription in breast cancer cells via a mechanism that involves protein–protein association with ERα. As a result of this interaction, the ability of ERα to transactivate the IGF-IR promoter is abrogated. These findings are consistent with a potential tumor suppressor role for WT1 in breast cancer and suggest that WT1 inactivation in tumoral cells may result in deregulated IGF-IR gene expression and enhanced mitogenic activation by locally produced and/or circulating IGFs.

Induction and processing of complex DNA damage in human breast cancer cells MCF-7 and nonmalignant MCF-10A cells

2008 ◽  
Vol 44 (4) ◽  
pp. 558-569 ◽  
Author(s):  
Dave C. Francisco ◽  
Prakash Peddi ◽  
Jessica M. Hair ◽  
Brittany A. Flood ◽  
Angela M. Cecil ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Mcf 7
Sign in / Sign up

Export Citation Format

Share Document