Therapeutic effects of bach1 siRNA on human breast adenocarcinoma cell line

Aletaha, Mansoor; Mansoori, Behzad; Mohammadi, Ali; Fazeli, Mehdi; Baradaran, Behzad

doi:10.1016/j.biopha.2017.01.030

Cited by 23 publications

(16 citation statements)

References 22 publications

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“…When the seeded cells reached to 50%-70% confluently, the cells were washed with PBS (phosphate-buffered saline) and the miR-193a-5p mimic transfection was performed using JetPEI reagent (Polyplus-transfection, Strasbourg, France). To find the appropriate dosage of transfected miRNA and optimal time, pilot assessments were carried out 19 in three 24, 48, 72 hours times intervals, and three dosages of 5, 7.5, 10 nmol to obtain the effective time and dosage, respectively. MiRNA from Caenorhabditis elegans (MISSION2® miRNA, Sigma-Aldrich Co.), with no sequence homology to the human gene, was used for transfection of negative controls (Table 1).…”

Section: Cell Culture and Transfectionsmentioning

confidence: 99%

Restoring of miR-193a-5p Sensitizes Breast Cancer Cells to Paclitaxel through P53 Pathway

et al. 2020

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Purpose : Recent evidence presented the important role of microRNAs in health and disease particularly in human cancers. Among those, miR-193 family contributes as a tumor suppressor in different benign and malignant cancers like breast cancer (BC) via interaction with specific targets. On the other hand, it was stated that miR-193 is able to modulate some targets in chemoresistant cancer cells. Therefore, the aim of this study was to evaluate the potential function of miR-193a-5p and paclitaxel in the apoptosis induction by targeting P53 in BC cells. Methods: At first, miR-193a-5p mimics were transfected to MDA-MB-231 BC cell line which indicated the lower expression level of miR-193a-5p. Subsequently, the transfected cells were treated with paclitaxel. Then, cell viability, apoptosis, and migration were evaluated by MTT, flow cytometry and DAPI staining, and scratch-wound motility assays, respectively. Moreover, the expression levels of P53 was evaluated by qRT-PCR. Results: The expression level of miR-193a-5p was restored in MDA-MB-231 cells which profoundly inhibited the proliferation (P<0.0001), induced apoptosis (P<0.0001) and harnessed migration (P<0.0001) in the BC cells and more effectiveness was observed in combination with paclitaxel. Interestingly, increased miR-193a-5p expression led to a reduction in P53 mRNA, offering that it can be a potential target of miR-193a. Conclusion: Taken together, it is concluded that the combination of miR-193a-5p restoration and paclitaxel could be potentially considered as an effective therapeutic strategy to get over chemoresistance during paclitaxel chemotherapy

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Section: Cell Culture and Transfectionsmentioning

confidence: 99%

Restoring of miR-193a-5p Sensitizes Breast Cancer Cells to Paclitaxel through P53 Pathway

et al. 2020

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“…Mansoor et al [28] found that the expression of miR-21 significantly decreased after silencing Bach1 gene with siRNA. Chen et al [29] reported that p38 expression decreased when miR-21 was overexpressed, and Lucia et al [30] found that when the expression level of miR-21 was increased, the expression level of Nrf2 significantly decreased.…”

Section: Biomed Research Internationalmentioning

confidence: 99%

A Systematic Review of the Various Effect of Arsenic on Glutathione Synthesis In Vitro and In Vivo

Ran

Liu

2020

BioMed Research International

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Background. Arsenic is a toxic metalloid widely present in nature, and arsenic poisoning in drinking water is a serious global public problem. Glutathione is an important reducing agent that inhibits arsenic-induced oxidative stress and participates in arsenic methylation metabolism. Therefore, glutathione plays an important role in regulating arsenic toxicity. In recent years, a large number of studies have shown that arsenic can regulate glutathione synthesis in many ways, but there are many contradictions in the research results. At present, the mechanism of the effect of arsenic on glutathione synthesis has not been elucidated. Objective. We will conduct a meta-analysis to illustrate the effects of arsenic on GSH synthesis precursors Glu, Cys, Gly, and rate-limiting enzyme γ-GCS in mammalian models, as well as the regulation of p38/Nrf2 of γ-GCS subunit GCLC, and further explore the molecular mechanism of arsenic affecting glutathione synthesis. Results. This meta-analysis included 30 studies in vivo and 58 studies in vitro, among which in vivo studies showed that arsenic exposure could reduce the contents of GSH (SMD=−2.86, 95% CI (-4.45, -1.27)), Glu (SMD=−1.11, 95% CI (-2.20,-0.02)), and Cys (SMD=−1.48, 95% CI (-2.63, -0.33)), with no statistically significant difference in p38/Nrf2, GCLC, and GCLM. In vitro studies showed that arsenic exposure increased intracellular GSH content (SMD=1.87, 95% CI (0.18, 3.56)) and promoted the expression of p-p38 (SMD=4.19, 95% CI (2.34, 6.05)), Nrf2 (SMD=4.60, 95% CI (2.34, 6.86)), and GCLC (SMD=1.32, 95% CI (0.23, 2.41)); the p38 inhibitor inhibited the expression of Nrf2 (SMD=−1.27, 95% CI (-2.46, -0.09)) and GCLC (SMD=−5.37, 95% CI (-5.37, -2.20)); siNrf2 inhibited the expression of GCLC, and BSO inhibited the synthesis of GSH. There is a dose-dependent relationship between the effects of exposure on GSH in vitro. Conclusions. These indicate the difference between in vivo and in vitro studies of the effect of arsenic on glutathione synthesis. In vivo studies have shown that arsenic exposure can reduce glutamate and cysteine levels and inhibit glutathione synthesis, while in vitro studies have shown that chronic low-dose arsenic exposure can activate the p38/Nrf2 pathway, upregulate GCLC expression, and promote glutathione synthesis.

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“…In fact, a previous study has shown that Bach1 can function as both an activator and a repressor of transcription on the same gene, depending on the cellular context [ 1 ]. Therefore, while some evidence suggests that Bach1 inhibition may be an effective therapeutic approach for the treatment of breast cancer [ 60 ], the role of Bach1 in cancer growth, progression, and metastasis appears to vary and must be thoroughly characterized for each type of cancer at different stages of tumor progression.…”

Section: Bach1 In Cancermentioning

confidence: 99%

Bach1: Function, Regulation, and Involvement in Disease

Zhang

Guo

Wei

et al. 2018

Oxidative Medicine and Cellular Longevity

114

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The transcription factor BTB and CNC homology 1 (Bach1) is widely expressed in most mammalian tissues and functions primarily as a transcriptional suppressor by heterodimerizing with small Maf proteins and binding to Maf recognition elements in the promoters of targeted genes. It has a key regulatory role in the production of reactive oxygen species, cell cycle, heme homeostasis, hematopoiesis, and immunity and has been shown to suppress ischemic angiogenesis and promote breast cancer metastasis. This review summarizes how Bach1 controls these and other cellular and physiological and pathological processes. Bach1 expression and function differ between different cell types. Thus, therapies designed to manipulate Bach1 expression will need to be tightly controlled and tailored for each specific disease state or cell type.

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Therapeutic effects of bach1 siRNA on human breast adenocarcinoma cell line

Cited by 23 publications

References 22 publications

Restoring of miR-193a-5p Sensitizes Breast Cancer Cells to Paclitaxel through P53 Pathway

Restoring of miR-193a-5p Sensitizes Breast Cancer Cells to Paclitaxel through P53 Pathway

A Systematic Review of the Various Effect of Arsenic on Glutathione Synthesis In Vitro and In Vivo

Bach1: Function, Regulation, and Involvement in Disease

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