scholarly journals Integrated molecular analysis of Tamoxifen-resistant invasive lobular breast cancer cells identifies MAPK and GRM/mGluR signaling as therapeutic vulnerabilities

2018 ◽  
Vol 471 ◽  
pp. 105-117 ◽  
Author(s):  
Hillary Stires ◽  
Mary M. Heckler ◽  
Xiaoyong Fu ◽  
Zhao Li ◽  
Catherine S. Grasso ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Molecular Analysis ◽  
Breast Cancer Cells ◽  
Lobular Breast Cancer ◽  
Tamoxifen Resistant ◽  
Invasive Lobular Breast Cancer

scholarly journals The role of AKR1 family in tamoxifen resistant invasive lobular breast cancer based on data mining

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Dong Xu ◽  
Yiqi Zhang ◽  
Feng Jin
Keyword(s):  
Breast Cancer ◽  
Data Mining ◽  
Cancer Cells ◽  
Differentially Expressed Genes ◽  
Breast Cancer Cells ◽  
Lobular Breast Cancer ◽  
Hub Genes ◽  
Tamoxifen Resistant ◽  
Invasive Lobular Breast Cancer

Abstract Background Tamoxifen (TAM) resistance to invasive lobular cell carcinoma is a challenge for breast cancer treatment. This study explored the role of Aldo-keto reductase family 1 (AKR1) family in tamoxifen-resistant aggressive lobular breast cancer based on data mining. Methods TAM-resistant invasive lobular breast cancer gene chip was downloaded from the Gene Expression Omnibus (GEO) database (accession-numbered as GSE96670). The online analytical tool GEO2R was used to screen for differentially expressed genes in TAM-resistant invasive lobular breast cancer cells and TAM-sensitive counterparts. A protein-protein interaction (PPI) networks were constructed using the STRING online platform and the Cytoscape software. GeneMANIA and GSCALite online tools were used to reveal the potential role of these hub genes in breast cancer progression and TAM resistance development. And the used the GSE67916 microarray data set to verify the differentially expression of these hub genes in breast cancer. The protein expression levels of AKR1C1, AKR1C2 and AKR1C3 in TAM-sensitive and resistant breast cancer cells were compared. The TAM sensitivity of breast cancer cells with or without AKR1C1, AKR1C2 or AKR1C3 gene manipulation was evaluated by cell viability assay. Results A total of 184 differentially expressed genes were screened. Compared with TAM sensitive breast cancer cells, 162 were up-regulated and 22 were down-regulated. The study identified several hub genes in the PPI network that may be involved in the development of TAM resistance of breast cancer, including signal transducer and activator of transcription 1 (STAT1), estrogen receptor alpha (ESR1), fibronectin1 (FN1), cytochrome P4501B1 (CYP1B1), AKR1C1, AKR1C2, AKR1C3 and uridine diphosphate glucuronosyltransferase (UGT) 1A family genes (UGT1A1, UGT1A3, UGT1A4, UGT1A6, UGT1A7, UGT1A8, UGT1A9, UGT1A10). Compared with TAM-sensitive counterparts, the expression levels of AKR1C1, AKR1C2, and AKR1C3 were up-regulated in TAM-resistant breast cancer cells. Conclusions Overexpression of each of these three genes significantly increased the resistance of breast cancer cells to TAM treatment, while their knockdown showed opposite effects, indicating that they are potential therapeutic target for the treatment of TAM-resistant breast cancer.

ABCB1/MDR1 contributes to the anticancer drug-resistant phenotype of IPH-926 human lobular breast cancer cells

2012 ◽  
Vol 315 (2) ◽  
pp. 153-160 ◽  
Author(s):  
Till Krech ◽  
Elisa Scheuerer ◽  
Robert Geffers ◽  
Hans Kreipe ◽  
Ulrich Lehmann ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Anticancer Drug ◽  
Breast Cancer Cells ◽  
Drug Resistant ◽  
Lobular Breast Cancer ◽  
Resistant Phenotype ◽  
Drug Resistant Phenotype

scholarly journals Differential effect of EGFR inhibitors on tamoxifen-resistant breast cancer cells

2015 ◽  
Vol 34 (3) ◽  
pp. 1613-1619 ◽  
Author(s):  
SANGMIN KIM ◽  
JEONGMIN LEE ◽  
SOO JIN OH ◽  
SEOK JIN NAM ◽  
JEONG EON LEE
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Differential Effect ◽  
Breast Cancer Cells ◽  
Egfr Inhibitors ◽  
Tamoxifen Resistant

scholarly journals Activated Farnesoid X Receptor inhibits growth of tamoxifen‐resistant breast cancer cells.

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Cinzia Giordano ◽  
Donatella Vizza ◽  
Salvatore Panza ◽  
Ines Barone ◽  
Daniela Bonofiglio ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Farnesoid X Receptor ◽  
Tamoxifen Resistant

scholarly journals Poly-ADP-Ribosylation of Estrogen Receptor-Alpha by PARP1 Mediates Antiestrogen Resistance in Human Breast Cancer Cells

Cancers ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 43 ◽  
Author(s):  
Nicholas Pulliam ◽  
Jessica Tang ◽  
Weini Wang ◽  
Fang Fang ◽  
Riddhi Sood ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Target Genes ◽  
Tamoxifen Resistance ◽  
Tamoxifen Treatment ◽  
Dependent Manner ◽  
Tamoxifen Resistant

Therapeutic targeting of estrogen receptor-α (ERα) by the anti-estrogen tamoxifen is standard of care for premenopausal breast cancer patients and remains a key component of treatment strategies for postmenopausal patients. While tamoxifen significantly increases overall survival, tamoxifen resistance remains a major limitation despite continued expression of ERα in resistant tumors. Previous reports have described increased oxidative stress in tamoxifen resistant versus sensitive breast cancer and a role for PARP1 in mediating oxidative damage repair. We hypothesized that PARP1 activity mediated tamoxifen resistance in ERα-positive breast cancer and that combining the antiestrogen tamoxifen with a PARP1 inhibitor (PARPi) would sensitize tamoxifen resistant cells to tamoxifen therapy. In tamoxifen-resistant vs. -sensitive breast cancer cells, oxidative stress and PARP1 overexpression were increased. Furthermore, differential PARylation of ERα was observed in tamoxifen-resistant versus -sensitive cells, and ERα PARylation was increased by tamoxifen treatment. Loss of ERα PARylation following treatment with a PARP inhibitor (talazoparib) augmented tamoxifen sensitivity and decreased localization of both ERα and PARP1 to ERα-target genes. Co-administration of talazoparib plus tamoxifen increased DNA damage accumulation and decreased cell survival in a dose-dependent manner. The ability of PARPi to overcome tamoxifen resistance was dependent on ERα, as lack of ERα-mediated estrogen signaling expression and showed no response to tamoxifen-PARPi treatment. These results correlate ERα PARylation with tamoxifen resistance and indicate a novel mechanism-based approach to overcome tamoxifen resistance in ER+ breast cancer.

scholarly journals Naringenin Inhibits Proliferation and Survival of Tamoxifen‐ Resistant Breast Cancer Cells

10.5772/66698 ◽  
2017 ◽  
Author(s):  
Joseph Ramos ◽  
Talia Hatkevich ◽  
Lauren Eanes ◽  
Idalys Santos-Sanchez ◽  
Yashomati M. Patel
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Tamoxifen Resistant
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