miR-192 enhances sensitivity of methotrexate drug to MG-63 osteosarcoma cancer cells

Bazavar, Mohammadreza; Fazli, Jafar; Valizadeh, Amir; Ma, Bo; Mohammadi, Erfan; Asemi, Zatollah; Alemi, Forough; Maleki, Masoomeh; Xing, Shilong; Yousefi, Bahman

doi:10.1016/j.prp.2020.153176

Cited by 25 publications

(17 citation statements)

References 29 publications

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“…MicroRNAs (miRNAs/miRs) can directly suppress the target gene translation by binding to the 3′ untranslated region (3′ UTR) of the target mRNA (Bazavar et al., 2020; Liang et al., 2020; Singh et al., 2012). Dysregulation of miRNAs promotes malignant phenotypes, such as tumour growth, metastasis and appearance of MDR through regulating downstream targets and associated pathways (Mutlu et al., 2016).…”

Section: Introductionmentioning

confidence: 99%

“…Dysregulation of miRNAs promotes malignant phenotypes, such as tumour growth, metastasis and appearance of MDR through regulating downstream targets and associated pathways (Mutlu et al, 2016). Increasing evidence confirms the correlation between miRNAs expression and chemo-resistance in numerous types of tumours (Bazavar et al, 2020;Tomimaru et al, 2010). For instance, the expression of miR-34a alleviated chemo-resistance in PCa cells (Fujita et al, 2008;Xu et al, 2016) or the expression of miR-122 significantly increased sensitivity to DOX and sorafenib in hepatocellular carcinoma cells (Fornari et al, 2009).…”

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confidence: 97%

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miR‐21 inhibition reverses doxorubicin‐resistance and inhibits PC3 human prostate cancer cells proliferation

Zhao

Ning²,

Wang

et al. 2021

Andrologia

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Many approaches have been examined to reversing multidrug resistance (MDR), but sub‐optimal target‐based strategies have limited their efficacy. Herein, we investigate microRNA (miR‐21) suppression on the doxorubicin (DOX)‐sensitisation of the DOX‐resistant (PC3/DOX) cell line in prostate cancer (PCa). Expression levels of miR‐21, P‐glycoprotein (P‐gp), MDR‐1 and PTEN evaluated in PC3/DOX cancer cells by qRT‐PCR and western blot analyses. The cytotoxic effects of transfected of miR‐21 were assessed by MTT assay for 72 hr. Rhodamine123 (Rh123) assay was employed to define the activity of P‐gp. Apoptosis was detected by Flow cytometry. As expected, miR‐21 was expressed highly in PC3/DOX cells (p < 0.05). It was shown that miRNA‑21 suppression considerably hindered PC3/DOX cell viability. miR‑21 suppression dramatically downregulated P‐gp expression and activity in DOX‐resistance cells and abolished MDR by an increment of intracellular accumulation of DOX in PC3/DOX cells (p < 0.05). PTEN is a key modulator of the PI3K/Akt/P‐gp cascade, which miR‐21 suppression led to the upregulation of PTEN and sequentially lower‐expression of P‐gp that reversed MDR. Also, miR‐21 repression enhanced the apoptosis rate of PC3/DOX cells. The findings of this paper contribute to the current understanding of the functions of miR‐21 in MDR‐reversing in PCa.

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Section: Introductionmentioning

confidence: 99%

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confidence: 97%

miR‐21 inhibition reverses doxorubicin‐resistance and inhibits PC3 human prostate cancer cells proliferation

Zhao

Ning²,

Wang

et al. 2021

Andrologia

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“…Based on the fact that MCL patients on ibrutinib have a high risk of recurrence and patients on ibrutinib who experience relapse have adverse outcomes, it is important to identify drug resistance mechanisms and relevant solutions. miRNA expression disorder is one of the major causes of drug resistance [9,[21][22][23][24][25][26][27][28][29][30][31] . Identifying the function of miRNA-223-3p as an upstream regulator of non-classical NF-κB signaling pathway in ibrutinib resistance in MCL is a significant advance, which might lead to rational combination therapy development to treat or prevent drug-resistant disease.…”

Section: Discussionmentioning

confidence: 99%

miRNA-223-3p modulates ibrutinib resistance through regulation of the CHUK/Nf-κb signaling pathway in mantle cell lymphoma

Yuan

Zhang

et al. 2021

Experimental Hematology

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This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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“…Studies are currently concentrating on scrutinising the new insights into molecular modifications in PCa noninvasive biomarkers, such as microRNAs (miRNAs/miRs), and biofluids, which have significant potential novel tumour biomarkers (Fendler et al., 2016). miRNAs are a class of 19 to 25 nucleotide (∼22 nt) noncoding RNA (ncRNA) oligonucleotides that negatively control the expression of different types of genes at the post‐transcriptional level mainly by directly binding the 3′‐untranslated regions (3′‐UTRs) of matching mRNA targets (Bazavar et al., 2020; Shi et al., 2020). miRNAs represent the most explored side of the ‘dark’ matter of the genome, which can act as oncogenes or tumour suppressors (Berindan‐Neagoe et al., 2014).…”

Section: Introductionmentioning

confidence: 99%

MiR‐622 acts as a tumor suppressor to induce cell apoptosis and inhibit metastasis in human prostate cancer

et al. 2021

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Growing evidence indicating the critical modulator roles of microRNAs (miRNAs) involved in prostate cancer (PCa) metastasis that holds great promise as therapeutic targets. Herein, we transfected the miR‐622 mimic into PC3 cells and evaluated the effects of this interference on these tumour cells' growth and the expression of specific metastatic genes. Transfecting of miR‐622 mimic and inhibitor, negative control (NC) inhibitor and NC was established using Lipofectamine 2000. The mRNA levels of miR‐622 and metastatic genes were evaluated using the qRT‐PCR and Western blot. Cytotoxic effects of miR‐622 were assessed by MTT. Apoptosis was detected using an ELISA cell death assay kit. miR‐622 is down‐regulated in PC3 cells. As expected, cell viability effects after transfection were described as miR‐622 inhibitor >NC and NC inhibitor >miR‐622 mimic (p < .01). Importantly, we showed that transfected miR‐622 mimic could enhance the apoptosis of PC3 cells, while transfected miR‐622 inhibitor could decrease cell apoptosis (p < .01). Furthermore, miR‐622 overexpression could increase significantly down‐regulated the MMP2, MMP9, CXCR‐4, c‐Myc and K‐Ras expression levels. Findings demonstrate a novel mechanism by which miR‐622 modulates PCa cells' metastasis by targeting metastatic genes. These data confirm the tumour‐suppressive function of miR‐622 in PCa cells by enhancing apoptosis and reducing metastasis.

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miR-192 enhances sensitivity of methotrexate drug to MG-63 osteosarcoma cancer cells

Cited by 25 publications

References 29 publications

miR‐21 inhibition reverses doxorubicin‐resistance and inhibits PC3 human prostate cancer cells proliferation

miR‐21 inhibition reverses doxorubicin‐resistance and inhibits PC3 human prostate cancer cells proliferation

miRNA-223-3p modulates ibrutinib resistance through regulation of the CHUK/Nf-κb signaling pathway in mantle cell lymphoma

MiR‐622 acts as a tumor suppressor to induce cell apoptosis and inhibit metastasis in human prostate cancer

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