The determination of changes in the expression of genes for selected specific transcriptional factors in in vitro ductal breast cancer cells under the influence of paclitaxel

Ziaja‐Sołtys, Marta; Rzymowska, Jolanta

doi:10.2478/s11658-011-0026-8

Cited by 3 publications

(4 citation statements)

References 40 publications

(35 reference statements)

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“…In this study, the starting concentration selected for testing was 25 nmol/L for both taxanes, since it was in the pharmacological range and a concentration that were shown by previous in vitro studies to have cytotoxic effects on breast cancer cells. [11][12][13][14][15][16][17][18][19][20] According to this, the final concentrations of the diluted solutions in our culture conditions equate to approximately molar concentrations of 12.5 Â 10 À17 , 12.5 Â 10 À21 and 12.5 Â 10 À41 mol/L for both taxanes.…”

Section: Discussionmentioning

confidence: 88%

“…It has been shown that the concentrations within the range of µmol/L to nmol/L of these drugs could alter mRNA and microRNA expression levels of various genes in cancer cells in vitro. [11][12][13][14][15][16][17][18] The studies demonstrated that most mRNAs and microRNAs were either up-regulated or down-regulated in a concentration-and time-dependent manner by taxane treatment of various cancer cell lines including human breast cancer cell line MCF-7. Given the knowledge that many genetic regulatory reactions occur at extremely low concentrations, gene expression data from tumor cells treated with extremely low doses or high dilution of taxanes may provide useful suggestions about biological responses of cells to anti-cancer treatment.…”

Section: Introductionmentioning

confidence: 99%

“…The starting concentration selected for testing was 25 nmol/L paclitaxel or docetaxel as related to pharmacological concentration and previous in vitro studies. [11][12][13] Five genes, namely p53 (tumor protein p53 [TP53], NM_000546), p21 (cyclin-dependent kinase inhibitor 1A, NM_078467), COX-2 (prostaglandinendoperoxide synthase 2, NM_000963), TUBB2A (class IIa b-tubulin, NM_001069) and TUBB3 (class III b-tubulin, NM_006086), which have critical roles in regulation of tumor cell proliferation, survival, inflammation and angiogenesis, were selected as the target genes from among those showing up-or down-regulation at pharmacological doses of taxanes, according to earlier studies. [13][14][15] On the other hand, we also evaluated the effects of these concentrations of both drugs on microtubule organization and cell cytotoxicity.…”

Section: Introductionmentioning

confidence: 99%

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Evidence that Extreme Dilutions of Paclitaxel and Docetaxel Alter Gene Expression of In Vitro Breast Cancer Cells

et al. 2018

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Section: Discussionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Evidence that Extreme Dilutions of Paclitaxel and Docetaxel Alter Gene Expression of In Vitro Breast Cancer Cells

et al. 2018

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“…Having improved our knowledge of cancer biology notwithstanding, treatment of breast cancer has remained a challenging issue [ 5 – 7 ]. Of interest, the molecular anomaly of breast cancer cells cannot be explained via the genetic background as a result of the frequent sporadicity associated with the cancer [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

The role of epigenetic modifications in drug resistance and treatment of breast cancer

et al. 2022

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Background Breast cancer is defined as a biological and molecular heterogeneous disorder that originates from breast cells. Genetic predisposition is the most important factor giving rise to this malignancy. The most notable mutations in breast cancer occur in the BRCA1 and BRCA2 genes. Owing to disease heterogeneity, lack of therapeutic target, anti-cancer drug resistance, residual disease, and recurrence, researchers are faced with challenges in developing strategies to treat patients with breast cancer. Results It has recently been reported that epigenetic processes such as DNA methylation and histone modification, as well as microRNAs (miRNAs), have potently contributed to the pathophysiology, diagnosis, and treatment of breast cancer. These observations have persuaded researchers to move their therapeutic approaches beyond the genetic framework toward the epigenetic concept. Conclusion Herein we discuss the molecular and epigenetic mechanisms underlying breast cancer progression and resistance as well as various aspects of epigenetic-based therapies as monotherapy and combined with immunotherapy.

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A review of epigenetic and gene expression alterations associated with intracranial meningiomas

He¹,

Pham²,

Pease³

et al. 2013

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Object A more comprehensive understanding of the epigenetic abnormalities associated with meningioma tumorigenesis, growth, and invasion may provide useful targets for molecular classification and development of targeted therapies for meningiomas. Methods The authors performed a review of the current literature to identify the epigenetic modifications associated with the formation and/or progression of meningiomas. Results Several epigenomic alterations, mainly pertaining to DNA methylation, have been associated with meningiomas. Hypermethylation of TIMP3 inactivates its tumor suppression activity while CDKN2 (p14[ARF]) and TP73 gene hypermethylation and HIST1H1c upregulation interact with the p53 regulation of cell cycle control. Other factors such as HOX, IGF, WNK2, and TGF-β epigenetic modifications allow either upregulation or downregulation of critical pathways for meningioma development, progression, and recurrence. Conclusions Genome-wide methylation profiling demonstrated that global hypomethylation correlates with tumor grades and severity. Identification of additional epigenetic changes, such as histone modification and higher-order chromosomal structure, may allow for a more thorough understanding of tumorigenesis and enable future individualized treatment strategies for meningiomas.

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The determination of changes in the expression of genes for selected specific transcriptional factors in in vitro ductal breast cancer cells under the influence of paclitaxel

Cited by 3 publications

References 40 publications

Evidence that Extreme Dilutions of Paclitaxel and Docetaxel Alter Gene Expression of In Vitro Breast Cancer Cells

Evidence that Extreme Dilutions of Paclitaxel and Docetaxel Alter Gene Expression of In Vitro Breast Cancer Cells

The role of epigenetic modifications in drug resistance and treatment of breast cancer

A review of epigenetic and gene expression alterations associated with intracranial meningiomas

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