&lt;p&gt;Overview of microRNA-199a Regulation in Cancer&lt;/p&gt;

Wang, Qiwen; Ye, Bingyu; Wang, Ping; Yao, Fenjie; Zhang, Chunyan; Yu, Guoying

doi:10.2147/cmar.s231971

Cited by 56 publications

(39 citation statements)

References 71 publications

(87 reference statements)

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“…ROS have been shown to induce angiogenesis to support tumor growth by suppressing miR-199a-5p in arsenic-treated (As-T) human bronchial epithelial cells [149]. MiR-199a-5p has been involved in several carcinogenic processes, i.e., proliferation, migration, invasion, apoptosis, autophagy, and glycol-metabolism [150]. Of interest, a protective role for miR-199a-5p has been described in I/R injured cardiomyocytes, while in the lung it has been shown to play a role in development and fibrosis [151,152].…”

Section: Crosstalk Between Mirnas and Ros To Support Lung Cancer Growthmentioning

confidence: 99%

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

Climent

Viggiani

Lin

et al. 2020

IJMS

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Reactive oxygen species (ROS) affect many cellular functions and the proper redox balance between ROS and antioxidants contributes substantially to the physiological welfare of the cell. During pathological conditions, an altered redox equilibrium leads to increased production of ROS that in turn may cause oxidative damage. MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level contributing to all major cellular processes, including oxidative stress and cell death. Several miRNAs are expressed in response to ROS to mediate oxidative stress. Conversely, oxidative stress may lead to the upregulation of miRNAs that control mechanisms to buffer the damage induced by ROS. This review focuses on the complex crosstalk between miRNAs and ROS in diseases of the cardiac (i.e., cardiac hypertrophy, heart failure, myocardial infarction, ischemia/reperfusion injury, diabetic cardiomyopathy) and pulmonary (i.e., idiopathic pulmonary fibrosis, acute lung injury/acute respiratory distress syndrome, asthma, chronic obstructive pulmonary disease, lung cancer) compartments. Of note, miR-34a, miR-144, miR-421, miR-129, miR-181c, miR-16, miR-31, miR-155, miR-21, and miR-1/206 were found to play a role during oxidative stress in both heart and lung pathologies. This review comprehensively summarizes current knowledge in the field.

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Section: Crosstalk Between Mirnas and Ros To Support Lung Cancer Growthmentioning

confidence: 99%

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

Climent

Viggiani

Lin

et al. 2020

IJMS

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“…In addition, regulatory role of miR-199a from adipose tissue-derived MSCs has also been reported to enhance the chemosensitivity in hepatocellular carcinoma through mTOR pathway 47 . Notably, miRNAs have different target genes in various diseases and exert diverse regulatory functions 48 , 49 . In this study, we have shown that in vivo delivery of agomir produced mature miR-199a-5p in recipient cells and significantly reduced Sirt1 expression, resulting increased MRL/ lpr splenic CD4+ T cell senescence.…”

Section: Discussionmentioning

confidence: 99%

Human umbilical cord-derived mesenchymal stem cell therapy ameliorate lupus through increasing CD4+ T cell senescence via MiR-199a-5p/Sirt1/p53 axis

Tien¹,

Ding²,

Liu³

et al. 2021

Theranostics

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Rationale : Although human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) transplantation has been proved to be an effective therapeutic approach to treat systemic lupus erythematosus (SLE), the detailed underlying mechanisms are not fully understood. Transferring miRNAs is one mean by which MSCs communicate with surrounding cells. Sirt1 is a NAD-dependent deacetylase that protects against cell senescence by deacetylating p53. Here we aimed to explore whether hUC-MSCs affected senescence of splenic CD4+ T cells through regulating Sirt1/p53 via miRNA in the MRL/ lpr lupus mouse model. Methods : The effects of hUC-MSCs on lupus syndrome and senescence pathways in MRL/ lpr mice in vivo and in vitro were determined. The functional roles of miR-199a-5p in splenic CD4+ T cell senescence were studied by miRNA mimic or inhibitor in vitro. MRL /lpr mice were injected with miR-199a-5p agomir to evaluate the effects of miR-199a-5p on splenic CD4+ T cell senescence and disease in vivo. Results : We showed that hUC-MSCs transplantation ameliorated lupus symptoms and increased senescence of splenic CD4+ T cells through Sirt1/p53 signaling via miR-199a-5p in MRL/ lpr mice. Moreover, systemic delivery of miR-199a-5p in MRL/ lpr mice increased splenic CD4+ T-cell senescence, mimicking the therapeutic effects of transplanted hUC-MSCs. Conclusions : We have identified miR-199a-5p as one of the mechanisms employed by hUC-MSCs to alleviate lupus disease associated pathologies in MRL/ lpr mice, which is attributable for promoting splenic CD4+ T cell senescence through Sirt1/p53 pathway.

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“…Thus, these miRNAs are abundantly expressed in normal liver [27] and seven of them (miR-122, let-7a, miR-22, -125b, -143, -194 and -24) are within the first 20 liver-specific miRNAs called "atlas liver" [30]. The expression levels of miR-122, let-7a, miR-22, -125b, -143, -194 and -199a have been described to be downregulated in liver cancer cells and function as tumor suppressor miRNAs, as these miRNAs are involved in inhibiting proliferation, cell cycle progression, epithelial-mesenchymal transition and activating apoptosis and autophagy [22,[31][32][33][34][35][36][37][38]. On the contrary, miR-21, -24, -210 and -224 have been reported to be upregulated in HCC and function as oncomiRs, promoting proliferation, cell cycle progression, biliary tumor growth, angiogenesis and aggressiveness [31,[39][40][41][42].…”

Section: Discussionmentioning

confidence: 99%

The Effect of Methylselenocysteine and Sodium Selenite Treatment on microRNA Expression in Liver Cancer Cell Lines

Lendvai

Szekerczés

Kontsek

et al. 2020

Pathol. Oncol. Res.

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The unique character of selenium compounds, including sodium selenite and Se-methylselenocysteine (MSC), is that they exert cytotoxic effects on neoplastic cells, providing a great potential for treating cancer cells being highly resistant to cytostatic drugs. However, selenium treatment may affect microRNA (miRNA) expression as the pattern of circulating miRNAs changed in a placebo-controlled selenium supplement study. This necessitates exploring possible changes in the expression profiles of miRNAs. For this, miRNAs being critical for liver function were selected and their expression was measured in hepatocellular carcinoma (HLE and HLF) and cholangiocarcinoma cell lines (TFK-1 and HuH-28) using individual TaqMan MicroRNA Assays following selenite or MSC treatments. For establishing tolerable concentrations, IC 50 values were determined by performing SRB proliferation assays. The results revealed much lower IC 50 values for selenite (from 2.7 to 11.3 μM) compared to MSC (from 79.5 to 322.6 μM). The treatments resulted in cell line-dependent miRNA expression patterns, with all miRNAs found to show fold change differences; however, only a few of these changes were statistically different in treated cells compared to untreated cells below IC 50. Namely, miR-199a in HLF, miR-143 in TFK-1 upon MSC treatment, miR-210 in HLF and TFK-1, miR-22,-24,-122, −143 in HLF upon selenite treatment. Fold change differences revealed that miR-122 with both selenium compounds, miR-199a with MSC and miR-22 with selenite were affected. The miRNAs showing minimal alterations included miR-125b and miR-194. In conclusion, our results revealed moderately altered miRNA expression in the cell lines (less alterations following MSC treatment), being miR-122, −199a the most affected and miR-125b,-194 the least altered miRNAs upon selenium treatment.

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<p>Overview of microRNA-199a Regulation in Cancer</p>

Cited by 56 publications

References 71 publications

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

Human umbilical cord-derived mesenchymal stem cell therapy ameliorate lupus through increasing CD4+ T cell senescence via MiR-199a-5p/Sirt1/p53 axis

The Effect of Methylselenocysteine and Sodium Selenite Treatment on microRNA Expression in Liver Cancer Cell Lines

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