Knockdown of microRNA‑29a regulates the expression of apoptosis‑related genes in MCF‑7 breast carcinoma cells

Khamisipour, Gholamreza; Mansourabadi, Elham; Naeimi, Behrouz; Moazzeni, Ali; Tahmasebi, Rahim; Hasanpour, Mojtaba; Mohammadi, Majid Mosahebi; Mansourabadi, Zahra; Shamsian, Shakib

doi:10.3892/mco.2017.1528

Cited by 9 publications

(11 citation statements)

References 37 publications

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“…In addition, it has been reported that upregulation of miR-29a may be implicated in cell apoptosis by targeting Mcl-1 expression in rat germ cell death (32). Previous studies have demonstrated that miR-29a is able to induce cell apoptosis by activating caspase proteins (33,34). For example, miR-29a was reported to be responsible for the activation of caspase-3-induced K562 cell apoptosis (35).…”

Section: Resultsmentioning

confidence: 99%

MicroRNA‑29a contributes to intracranial aneurysm by regulating the mitochondrial apoptotic pathway

Zhao

Zhang

2018

Mol Med Report

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Intracranial aneurysm (IA) is an abnormal expansion in the intracranial arteries that weakens the arterial wall by consistently pushing the vascular wall outwards, which leads to a higher risk of aneurysm rupture. A number of reports have demonstrated that apoptosis is associated with the growth and rupture of IA. MicroRNAs (miRNAs/miRs) perform vital roles in the regulation of the mitochondrial apoptotic pathway and signaling proteins. Increasing evidence has already revealed the role of miR‑29a in injury, including liver injury, cardiovascular injury and ischaemia‑reperfusion injury. However, the role of miR‑29a in IA remains unclear at present. The present study investigated the role of miR‑29a in IA pathogenesis and the underlying mechanisms. By using reverse transcription‑quantitative polymerase chain reaction and western blot analysis, the present study demonstrated that genes, including caspase‑3, ‑8 and ‑9, and proteins, including cytochrome c and myeloid cell leukemia 1 (Mcl‑1), involved in mitochondrial apoptosis pathways were upregulated in IA groups compared with controls. In addition, microarray analysis demonstrated that miR‑29a, one of the most altered miRs in IA mice, was overexpressed in IA mice compared with controls. In vitro experiments revealed that miR‑29a downregulation attenuated human brain vascular smooth muscle cell (HBVSMC) apoptosis, while miR‑29a overexpression increased the apoptosis of HBVSMCs. Furthermore, luciferase reporter analysis revealed that Mcl‑1 is a direct target gene of miR‑29a. An in vivo IA model confirmed that miR‑29a overexpression may promote apoptosis through mitochondrial pathways. It was therefore concluded that miR‑29a may contribute to the progression of IA by regulating mitochondrial apoptotic pathways. Thus, miR‑29a is a potential therapeutic target for IA.

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Section: Resultsmentioning

confidence: 99%

MicroRNA‑29a contributes to intracranial aneurysm by regulating the mitochondrial apoptotic pathway

Zhao

Zhang

2018

Mol Med Report

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“…On the other hand, many studies have shown that miRNAs may target components of this pathway and potentially inhibit their expression, thereby increasing malignancies (13,35). Moreover, BCL-2 acts as an apoptosis regulator and has been shown to play a critical role in the pathogenesis of various types of cancer (12).…”

Section: Discussionmentioning

confidence: 99%

“…Expression of p53, p21, and BCL-2 mRNA in Jurkat cells were quantified using a 2X Real MOD Green PCR Master Mix kit (Takara Bio, Inc., Otsu, Japan), according to the manufacturer's instructions. Briefly, 2 µL cDNA product was diluted in a final volume of 20 µL, containing 10 pmol of each primer, 10 µL 2× reaction mixture of SYBR Green and 7.4 µL sterile deionized water (12). The cycling program was as follows: An initial denaturation step at 95°C for 10 min, followed by 40 cycles including a denaturation step at 95°C for 10 sec, annealing and extension at 55°C for 40 sec.…”

Section: Rna Extraction and Quantitative Real-time Reverse Transcriptmentioning

confidence: 99%

“…However, some miRNAs act as oncogenes in cancers by negatively regulating tumor suppressor genes (10). Among these targets, the tumor suppressor genes p53 and p21 are particularly important, since they can be a direct target of miRNAs and regulate the expression and processing of them (11,12). It has been shown that these tumor suppressors can be inactivated by miRNAs overexpression in malignancies and may result in the development of cancerous phenotypes (12,13).…”

Section: Introductionmentioning

confidence: 99%

“…Among these targets, the tumor suppressor genes p53 and p21 are particularly important, since they can be a direct target of miRNAs and regulate the expression and processing of them (11,12). It has been shown that these tumor suppressors can be inactivated by miRNAs overexpression in malignancies and may result in the development of cancerous phenotypes (12,13). Therefore, it is important to identify dysregulated miRNAs and their targets for the detection of cancers and finding new therapeutic strategies (10).…”

Section: Introductionmentioning

confidence: 99%

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Overexpression of MicroRNA-506 in Jurkat (acute T Cell Leukemia) Cell Line

et al. 2020

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Scan to discover online Background & Objective: Acute lymphoblastic leukemia (ALL) is a malignant disease that arises from various mutations in B or T-lymphoid progenitors. MicroRNAs (miRNAs) regulate gene expression by binding to the 3' untranslated region of proteincoding genes. Dysregulation of miRNA expression may result in the development of cancerous phenotypes. Therefore, for the first time in this field, the present study aims to investigate the effect of overexpression of miR-506 in Jurkat (acute T cell leukemia) cell line. Methods: In this study, Jurkat cell lines were cultured in RPMI-1640 medium. Next, miR-506 was transfected with concentrations of 50 and 100 nM with Lipofectamine 2000. The accuracy of the transfection was confirmed by the transfection of siRNA conjugated with FITC. 48 h after transfection, the cells were prepared for other tests (flow cytometry, MTT assay, and RNA extraction). The expression level of miR-506 in the cells was analyzed using the quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). Finally, SPSS 21 software was used for the data analysis. Results: According to our results, the viability of cells in concentrations of 50 and 100 nM was significantly higher than the control group. By overexpression of miR-506, the expressions of pro-apoptotic genes (p53, p21) and anti-apoptotic gene B-cell lymphoma-2 (BCL-2) are decreased and increased, respectively. Conclusion: This study showed that miR-506 may function as an oncogenic miRNA in the TALL cell line. In conclusion, overexpression of miR-506 leads to an increase in viable cancer cells.

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The Potential Role of Zinc Oxide Nanoparticles in MicroRNAs Dysregulation in STZ-Induced Type 2 Diabetes in Rats

Othman

Hafez

Moneim

2019

Biol Trace Elem Res

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Diabetes mellitus (DM) is a group of metabolic disorders that are characterized by a loss of glucose homeostasis and insufficiency in production or action of insulin. Development of newly antidiabetic molecules using a variety of organic compounds and biomolecules has been in practice for a long time. Recently, nanomaterials are also being used in antidiabetic studies for their unique properties. In this context, zinc nanoparticles have drawn attention due to the relationship between diabetes and imbalance of zinc homeostasis. Few studies have attempted to investigate the effect of zinc oxide nanoparticles (ZON) in microRNA dysregulations in diabetes. To evaluate the therapeutic effect of ZON on streptozotocin (STZ)-induced diabetic rats as well as its role in microRNA dysregulations. Diabetes was induced in rats by 60 mg/kg body weight (bwt) of STZ and then treated with ZON (5 mg/kg bwt) for 15 consecutive days. The levels of glucose, insulin, oxidative stress markers, and microRNAs expression were measured in liver and pancreas tissues. Intraperitoneal injection of 60 mg/kg bwt of STZ to Wistar rats caused significant decreases in the body weight and Zn contents of pancreas, liver, and kidney. Also, STZ injection increased the blood glucose level and oxidative stress (lipid peroxidation (LPO) and nitric oxide (NO). Meanwhile, STZ decreased blood insulin and pancreatic anti-oxidants. STZ also resulted in β cell dysfunction and destruction and altered the expression of certain pancreatic and liver microRNAs. ZON treatment for 15 days, at a dose of 5 mg/kg bwt resulted in marked improvements in the blood insulin, glucose tolerance, and structure and function of the pancreatic β cells. Furthermore, ZON administration reduced LPO and NO, and increased the levels of enzymatic and non-enzymatic anti-oxidants in STZ-induced diabetic rats. It was found also that ZON specifically regulated the expression of pancreatic and liver microRNAs that involved in diabetes development. The obtained results revealed that ZON is a promising antidiabetic agent. The antidiabetic effect of ZON was partially mediated by restoring the oxidants/antioxidants balance and by modulating the alerted microRNAs

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Knockdown of microRNA‑29a regulates the expression of apoptosis‑related genes in MCF‑7 breast carcinoma cells

Cited by 9 publications

References 37 publications

MicroRNA‑29a contributes to intracranial aneurysm by regulating the mitochondrial apoptotic pathway

MicroRNA‑29a contributes to intracranial aneurysm by regulating the mitochondrial apoptotic pathway

Overexpression of MicroRNA-506 in Jurkat (acute T Cell Leukemia) Cell Line

The Potential Role of Zinc Oxide Nanoparticles in MicroRNAs Dysregulation in STZ-Induced Type 2 Diabetes in Rats

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