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Drug: Tamoxifen

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Total 112 results found since Jan 2013.

EZH2 knockdown in tamoxifen-resistant MCF-7 cells unravels novel targets for regaining sensitivity towards tamoxifen.
CONCLUSION: Overall, we propose that targeting EZH2 or the molecules down the cascade might be helpful in reacquiring sensitivity to tamoxifen in breast cancer. PMID: 32990923 [PubMed - as supplied by publisher]
Source: Breast Cancer - September 28, 2020 Category: Cancer & Oncology Authors: Kumari K, Kumar S, Parida DK, Mishra SK Tags: Breast Cancer Source Type: research

MST2 silencing induces apoptosis and inhibits tumor growth for estrogen receptor alpha-positive MCF-7 breast cancer.
Abstract Mammalian sterile 20-like kinase 1/2 (MST1/2) plays an important role in cell growth and apoptosis and functions as a tumor suppressor. Previously, we showed that MST2 overexpression activates Estrogen receptor alpha (ERα) in human breast cancer MCF-7 cells in the absence of a ligand. Here, we examined the role of MST2 in the growth of ER-positive MCF-7 cells. Cell cycle, apoptosis, and mammosphere formation assay method were implemented to detect the biological effects of MST2 ablation on the growth of MCF-7 cells in vitro. The effect of MST2-siRNA on MCF-7 cells tumor growth in vivo was studied in tumo...
Source: Toxicology and Applied Pharmacology - September 28, 2020 Category: Toxicology Authors: Park J, Kim GH, Lee J, Phuong BTC, Kong B, Won JE, Won GW, Lee YH, Han HD, Lee Y Tags: Toxicol Appl Pharmacol Source Type: research

Estrogen Receptor alpha depletion affects the biomechanical properties and cytoskeleton rearrangements in breast cancer cells.
In this study, we found that tamoxifen-resistant breast cancer cells (MCF-7/TamR) altered cell morphology and lacked of ERα expression during the process of the Tamoxifen resistance induction. To determine whether this change was influenced by ERα expression, we transiently constructed another ERα depleted model with ERα siRNA (MCF-7/ERα siRNA) and used atomic force microscope (AFM) to detect morphological and biophysical changes. The results indicated that the roughness and Young's modulus of ERα expression depleted cells were significantly increased, accompanied by rearrangement of the cytoskeletal proteins (F-acti...
Source: Biochemical and Biophysical Research communications - February 17, 2020 Category: Biochemistry Authors: Zhao C, Hou X, Peng Z, Sun X, Li E, Yang H, Lu Y, Zhu L Tags: Biochem Biophys Res Commun Source Type: research

GSE124655 FOXA1 upregulation promotes enhancer and transcriptional reprogramming in endocrine-resistant breast cancer RNA-seq
Contributors : Xiaoyong Fu ; Rachel Schiff ; Rinath Jeselsohn ; Myles BrownSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensForkhead box A1 (FOXA1) is a pioneer factor that facilitates chromatin binding and function of lineage-specific and oncogenic transcription factors. Here, we have demonstrated that FOXA1 overexpression in estrogen receptor-positive breast cancer cells drives genome-wide enhancer reprogramming to activate pro-metastatic transcriptional programs. We have identified the hypoxia-inducible transcription factor HIF-2 α as the top FOXA1-engaged super-enhancer target ind...
Source: GEO: Gene Expression Omnibus - December 18, 2019 Category: Genetics & Stem Cells Tags: Expression profiling by high throughput sequencing Homo sapiens Source Type: research

Cancers, Vol. 11, Pages 1858: FoxO3a as a Positive Prognostic Marker and a Therapeutic Target in Tamoxifen-Resistant Breast Cancer
Conclusions: Altogether, our data indicate that FoxO3a is a key target to be exploited in endocrine-resistant tumors. In this context, LTG, being able to induce FoxO3a, might represent a valid candidate in combination therapy to prevent resistance to tamoxifen in patients at risk.
Source: Cancers - November 24, 2019 Category: Cancer & Oncology Authors: Michele Pellegrino Pietro Rizza Ada Don à Alessandra Nigro Elena Ricci Marco Fiorillo Ida Perrotta Marilena Lanzino Cinzia Giordano Daniela Bonofiglio Rosalinda Bruno Federica Sotgia Michael P. Lisanti Diego Sisci Catia Morelli Tags: Article Source Type: research

TWIST1 transcriptionally regulates glycolytic genes to promote the Warburg metabolism in pancreatic cancer.
In this study, we found that the highly conserved transcription factor, TWIST1, is a crucial regulator of aerobic glycolysis in PDAC. Genetic silencing of TWIST1 significantly inhibited the glycolytic phenotypes of PDAC cells as revealed by reduced glucose uptake, lactate production, and extracellular acidification rate, which can be restored by re-expression of siRNA-resistant TWIST1. Moreover, tamoxifen-inducible expression of TWIST1 promoted the Warburg metabolism of PDAC cells. Mechanistically, by luciferase reporter assay and chromatin immunoprecipitation experiment, we showed that TWIST1 can directly increase the exp...
Source: Experimental Cell Research - November 5, 2019 Category: Cytology Authors: Wang XX, Yin GQ, Zhang ZH, Rong ZH, Wang ZY, Du DD, Wang YD, Gao RX, Xian GZ Tags: Exp Cell Res Source Type: research

Knockdown of PTEN decreases expression of estrogen receptor β and tamoxifen sensitivity of human breast cancer cells
In this study we examined whether expression of ER β in turn might be affected by tumor suppressor PTEN, analyzed the effect of this interaction on tamoxifen response and the co-expression of both genes in human breast cancer samples. After siRNA-mediated PTEN knockdown, Western blot analysis revealed a reduction of ER β protein expression by 67.2% in MCF-7 cells and by 73.6% in T-47D cells (both p<0.01), results which could be verified on the mRNA level. In cells with normal PTEN and ER β status, after 6 days of treatment with 1 µM 4-OH tamoxifen, E2-driven proliferation was decreased by 64.5% in MCF-7 and by 57.7...
Source: Steroids - October 9, 2019 Category: Drugs & Pharmacology Source Type: research

Resveratrol Promotes Diabetic Wound Healing via SIRT1-FOXO1-c-Myc Signaling Pathway-Mediated Angiogenesis
Conclusion: Our findings indicate that the positive role of RES in diabetic wound healing via its SIRT1-dependent endothelial protection and pro-angiogenic effects involves the inhibition of FOXO1 and the de-repression of c-Myc expression. Introduction Diabetes mellitus is a metabolic disease with an increasing incidence worldwide (Zimmet et al., 2014). The disease often leads to the development of serious complications such as microangiopathy, mainly including retinopathy, nephropathy, neuropathy, and diabetic non-healing skin ulcers (Zheng et al., 2018). Diabetic non-healing skin ulcers such as foot ulcers are ca...
Source: Frontiers in Pharmacology - April 23, 2019 Category: Drugs & Pharmacology Source Type: research

Complement C5b-9 and Cancer: Mechanisms of Cell Damage, Cancer Counteractions, and Approaches for Intervention
In conclusion, osmotic burst of inflated complement-damaged cells may occur, but these bursts are most likely a consequence of metabolic collapse of the cell rather than the cause of cell death. The Complement Cell Death Mediator: A Concerted Action of Toxic Moieties Membrane pores caused by complement were first visualized by electron microscopy on red blood cell membranes as large ring structures (22). Similar lesions were viewed on E. coli cell walls (23). Over the years, ample information on the fine ultrastructure of the MAC that can activate cell death has been gathered (24) and has been recently further examined (...
Source: Frontiers in Immunology - April 9, 2019 Category: Allergy & Immunology Source Type: research

Cancers, Vol. 11, Pages 189: Tumor-Associated Macrophages Induce Endocrine Therapy Resistance in ER+ Breast Cancer Cells
a Gil Antiestrogenic adjuvant treatments are first-line therapies in patients with breast cancer positive for estrogen receptor (ER+). Improvement of their treatment strategies is needed because most patients eventually acquire endocrine resistance and many others are initially refractory to anti-estrogen treatments. The tumor microenvironment plays essential roles in cancer development and progress; however, the molecular mechanisms underlying such effects remain poorly understood. Breast cancer cell lines co-cultured with TNF-&amp;alpha;-conditioned macrophages were used as pro-inflammatory tumor microenvironm...
Source: Cancers - February 6, 2019 Category: Cancer & Oncology Authors: Castellaro Rodriguez-Baili Di Tada Gil Tags: Article Source Type: research

Expression of the CD59 Glycoprotein Precursor is Upregulated in an Estrogen Receptor-alpha (ER- α)-Negative and a Tamoxifen-Resistant Breast Cancer Cell Line In Vitro.
CONCLUSIONS In summary, our results proposed a candidate biomarker for predicting TAM resistance in ERa-positive breast cancer via targeting CD59, therefore it could be a novel therapeutic option. PMID: 30391994 [PubMed - in process]
Source: Medical Science Monitor - November 7, 2018 Category: Research Tags: Med Sci Monit Source Type: research

GSE115270 Differential expression profiling of the TamR cells following AR knockdown
In this study, we sought to characterize the functional consequences of AR knockdown using a siRNA-mediated approach in a tamoxifen-resistant (TamR) derivative of MCF7 breast cancer cell line.
Source: GEO: Gene Expression Omnibus - June 5, 2018 Category: Genetics & Stem Cells Tags: Expression profiling by array Homo sapiens Source Type: research

PKD1 is a potential biomarker and therapeutic target in triple-negative breast cancer.
Authors: Spasojevic C, Marangoni E, Vacher S, Assayag F, Meseure D, Château-Joubert S, Humbert M, Karam M, Ricort JM, Auclair C, Regairaz M, Bièche I Abstract Protein Kinase D1 (PKD1) is a serine/threonine kinase encoded by the PRKD1 gene. PKD1 has been previously shown to be a prognostic factor in ERα+ tamoxifen-resistant breast tumors and PKD1 overexpression confers estrogen independence to ERα+ MCF7 cells. In the present study, our goal was to determine whether PKD1 is a prognostic factor and/or a relevant therapeutic target in breast cancer. We analyzed PRKD1 mRNA levels in 527 primary breast tumors. We fou...
Source: Oncotarget - May 31, 2018 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

GSE113092 GRHL2 is a key lineage determining factor which collaborates with FOXA1 to establish a targetable collateral pathway in the setting of endocrine therapy-resistant breast cancer ChIP-seq
Contributors : Jeff S Jasper ; Kimberly J Cocce ; Logan Everett ; Suzanne Wardell ; Thomas Westerling ; Taylor Krebs ; Robert Baldi ; Tricia M Wright ; Alex Yllanes ; Jeremy T Blitzer ; Craig Logsdon ; Daniel Rakiec ; David Ruddy ; Terry Hyslop ; Allison Hall ; Jeffrey R Marks ; Gregory E Crawford ; Myles Brown ; Donald P McdonnellSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensThe estrogen receptor (ER) is expressed in the majority of luminal breast cancers and inhibition of its transcriptional activity with selective estrogen receptor modulators, selective estrogen rec...
Source: GEO: Gene Expression Omnibus - April 13, 2018 Category: Genetics & Stem Cells Tags: Genome binding/occupancy profiling by high throughput sequencing Homo sapiens Source Type: research

GSE108167 GRHL2 is a key lineage determining factor which collaborates with FOXA1 to establish a targetable collateral pathway in the setting of endocrine therapy-resistant breast cancer DNase hypersensitivity
Contributors : Jeff S Jasper ; Kimberly J Cocce ; Logan Everett ; Suzanne Wardell ; Thomas Westerling ; Taylor Krebs ; Robert Baldi ; Tricia M Wright ; Alex Yllanes ; Jeremy T Blitzer ; Craig Logsdon ; Daniel Rakiec ; David Ruddy ; Terry Hyslop ; Allison Hall ; Jeffrey R Marks ; Gregory E Crawford ; Myles Brown ; Donald P McdonnellSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensThe estrogen receptor (ER) is expressed in the majority of luminal breast cancers and inhibition of its transcriptional activity with selective estrogen receptor modulators, selective estrogen rec...
Source: GEO: Gene Expression Omnibus - December 16, 2017 Category: Genetics & Stem Cells Tags: Genome binding/occupancy profiling by high throughput sequencing Homo sapiens Source Type: research