Expression Levels Of miR-26a Research Articles

The synergistic impact of sleep duration and obesity on metabolic syndrome risk: exploring the role of microRNAs

Introduction: Given the well-established association between metabolic syndrome (MetS) and obesity, this study elucidates the influences of sleep duration and weight on MetS risk and explores the potential role of miRNAs as underlying mechanisms. Methods: According to sleep logs and biochemistry tests, this study investigated the association between MetS and its components, sleep duration, and weight in four subgroups: A: normal sleepers with normal weight (N = 145), B: normal sleepers with obesity (N = 140), C: short sleepers with normal weight (N = 130), and D: short sleepers with obesity (N = 142). Chi-square, one-way ANOVA, and Tukey’s post hoc tests were used for statistical analysis. Furthermore, following total RNA isolation by TRIzol from blood samples, cDNA was synthesized using stem-loop technique. Quantitative real-time polymerase chain reaction (qRT-PCR) was then employed to evaluate the expression levels of miR-33a, miR-378a, miR-132-3p, and miR-181d. The data were analyzed using one-way ANOVA. Results: Our findings revealed the strongest association between MetS prevalence and individuals in group D (short sleepers with obesity; Cramer's V = 0.649, P < 0.001). This observation underscores the synergistic effect of short sleep and obesity on MetS risk. Furthermore, there was an independent association between short sleep duration and elevated triglyceride levels (P < 0.05). MicroRNA expression analysis revealed downregulation of miR-33a and miR-181d in B, C, and D groups compared to the normal group. Conversely, miR-132-3p expression was upregulated in the B, C, and D groups. Conclusion: Short sleep and obesity synergistically elevate MetS risk, potentially via miR-33a and miR-181d downregulation and miR-132-3p upregulation, impacting triglyceride metabolism.

Establishment of a myostatin gene-knockout C2C12 cell line and evaluation of related microRNA expression

The strategy of blocking myostatin (MSTN) signal transduction has long been regarded as a promising approach in the treatment of patients with muscle loss. However, individuals taking blocking agents often encounter issues such as lack of strength, fatigue, and poor muscle proliferation due to muscle hypertrophy and the involvement of multiple receptors. To address these challenges, a series of experiments were conducted on a C2C12 cell line in this study. First, the pX601-SaCas9-sgRNA/puro vector carrying a Cas9-encoded gene was constructed and subsequently used to produce Mstn-knockout (Mstn-KO) C2C12 cell lines. The expression level of the MSTN protein and the growth characteristics of the cell lines were verified. Moreover, the expression of muscle growth-related microRNAs in the cell lines was analyzed through real-time polymerase chain reaction (PCR). The results indicate that we have successfully established a method for constructing Mstn-KO cell lines with stable passage. No expression of the MSTN protein and strong cell proliferation were observed in the cell lines. Moreover, real-time PCR experiments showed that the expression levels of miR-1, miR-431, miR-206, and miR-133a were significantly increased (P < 0.01), the expression level of miR-23a was significantly increased (P < 0.05), and the expression level of miR-486 was significantly decreased (P < 0.05). These findings indicate that multiple miRNAs are closely associated with MSTN regulation. This study lays the foundation for further investigation into the effects of the Mstn gene on the physiological function of myoblasts and the development of drugs that block the MSTN signaling pathway.

Are miR-26a and miR-26b microRNAs potent prognostic markers of gestational diabetes?

Gestational diabetes mellitus is a common public health problem, accompanied by complications for the mother and fetus. So, introducing new biomarkers to identify early diabetes is essential. As serum miRNAs are potentially appropriate markers, we investigated miR-26a and miR-26b expression levels in pregnant women with and without gestational diabetes. Demographic and clinical characteristics of 40 gestational diabetic patients and 40 healthy controls were assessed. The expression level of miR-26a and miR-26b microRNAs was measured by real-time PCR. Statistical analysis was done with GraphPad Prism software (version 8.4.3). The findings of this study showed that the expression level of miR-26a and miR-26b increased in women with gestational diabetes compared with healthy pregnant women, but the increase in expression was only significant for miR-26a (p < 0.05). According to the statistical and ROC curves, we suggest miR-26a as a potential biomarker for the early diagnosis of gestational diabetes mellitus.

Epigenetics in Canine Mammary Tumors: Upregulation of miR-18a and miR-18b Oncogenes Is Associated with Decreased ERS1 Target mRNA Expression and ERα Immunoexpression in Highly Proliferating Carcinomas

The expression of miRNAs is one of the main epigenetic mechanisms responsible for the regulation of gene expression in mammals, and in cancer, miRNAs participate by regulating the expression of protein-coding cancer-associated genes. In canine mammary tumors (CMTs), the ESR1 gene encodes for ERα, and represents a major target gene for miR-18a and miR-18b, previously found to be overexpressed in mammary carcinomas. A loss in ERα expression in CMTs is commonly associated with poor prognosis, and it is noteworthy that the downregulation of the ESR1 would appear to be more epigenetic than genetic in nature. In this study, the expression of ESR1 mRNA in formalin-fixed, paraffin-embedded (FFPE) canine mammary tumors (CMTs) was evaluated and compared with the expression levels of miR18a and miR18b, both assessed via RT-qPCR. Furthermore, the possible correlation between the miRNA expression data and the immunohistochemical prognostic factors (ERα immunoexpression; Ki67 proliferative index) was explored. A total of twenty-six FFPE mammary samples were used, including 22 CMTs (7 benign; 15 malignant) and four control samples (three normal mammary glands and one case of lobular hyperplasia). The obtained results demonstrate that miR-18a and miR-18b are upregulated in malignant CMTs, negatively correlating with the expression of target ESR1 mRNA. Of note, the upregulation of miRNAs strictly reflects the progressive loss of ERα immunoexpression and increased tumor cell proliferation as measured using the Ki67 index. The results suggest a central role of miR-18a and miR-18b in the pathophysiology of canine mammary tumors as potential epigenetic mechanisms involved in ERα downregulation. Moreover, as miRNA expression reflects ERα protein status and a high proliferative index, miR-18a and miR-18b may represent promising biomarkers with prognostic value. More detailed investigations on a larger number of cases are needed to better understand the influence of these miRNAs in canine mammary tumors.

MiR-18a expression correlates with ATM and p53 levels and poor prognosis in lymphomas.

microRNAs (miRNAs) are non-coding, endogenous, small-molecule RNAs. They are involved in cell proliferation, differentiation, apoptosis, and metabolism. Additionally, they play an essential role in the development and progression of various malignancies. Recent research has revealed that miR-18a plays an important role in cancer development. However, its role in lymphoma is not yet fully understood. In this study, we investigated the clinicopathological characteristics and potential functional roles of miR-18a in lymphomas. First, we predicted the potential downstream genes of miR-18a using miRTarBase software and subjected these downstream genes to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses to determine the potential mechanisms of action of these genes. We found that these target genes were closely related to cellular senescence, the p53 signaling pathway, and other signaling pathways. From the predicted downstream target genes, ATM and p53 were selected as the target genes; their deletion in patients with lymphoma was detected using the fluorescence in situ hybridization technique. The results showed that some patients with lymphoma have a deletion of the ATM and p53 genes. In addition, the deletion rates of ATM and p53 were positively correlated with the expression of miR-18a. Next, the expression levels of miR-18a and the deletion rates of ATM and p53 were used for correlation and prognostic analyses with patient clinical information. The findings revealed a significant difference in disease-free survival (DFS) between patients with lymphoma with ATM deletion and those with a normal ATM gene expression (p < 0.001). Moreover, a significant difference in overall survival (OS) and DFS between patients with p53 deletion and those with normal p53 expression was observed (p < 0.001). The results indicate that the deletion of ATM and p53 downstream of miR-18a is closely associated with the development of lymphoma. Thus, these biomarkers may serve as key prognostic biomarkers for lymphomas.

GAS5 alleviates cisplatin drug resistance in oral squamous cell carcinoma by sponging miR-196a.

The long non-coding RNA Growth-arrest-specific transcript 5 (GAS5) has been extensively linked with the ability of cancer cells to resist chemotherapeutic interventions. This prospective study aimed to investigate the role of GAS5 in oral squamous cell carcinoma (OSCC), which has been poorly characterized to date. GAS5 and miR-196a expression levels were detected by quantitative real-time PCR analysis. Cisplatin (DDP) sensitivity and apoptosis levels were determined using Cell Counting Kit 8 and flow cytometry, respectively. Luciferase reporter and RNA immunoprecipitation assays were performed to confirm target miRNAs of GAS5. We found that GAS5 was expressed at low levels in DDP-resistant OSCC cell lines and tissues, and that GAS5 levels were intricately linked to the survival rates of OSCC patients. GAS5 overexpression led to the recovery of DDP sensitivity in CAL27/DDP cells. Additionally, in both DDP-resistant and -sensitive lines, GAS5 showed a cytoplasmic distribution and downregulated miR-196a in OSCC tissues. Exogenous transfection of miR-196a alleviated the effects of GAS5 on DDP sensitivity, confirming this as the mechanism of chemoresistance. These findings may provide new targets for the treatment of chemotherapy-resistant OSCC.

MicroRNA-26a confers a potential biomarker for screening of deep vein thrombosis

BackgroundDeep vein thrombosis (DVT) is one of the most common cardiovascular diseases caused by the formation of a clot in deep veins. The measurement of microRNAs (miRNAs) as diagnostic biomarkers in the blood and plasma confers a tool to detect human diseases without invasive methods. In this regard, the present study aimed to assess the changes in the expression level of miR-26a in patients with DVT in order to investigate its potential as prognostic biomarker in these subjects. MethodsThis study was performed on 200 patients with VDT and 200 healthy subjects, who were selected after matching for gender and age. The serum samples were obtained from study participants, RNA content of the samples was isolated, cDNA was synthesized, and the expression level of miR-26a was measured using Real-time PCR. ResultsDownregulation of miR-26a expression was detected in patients in comparison to normal group (Fold change = 0.32, P = 0.0004). Additionally, miR-26a expression was significantly lower in patients with emboli (Fold change = 0.27, P = 0.032) compared to those without emboli. ROC curve analysis of miR-26a revealed its potential as a biomarker for DVT (Area: 0.73, P = 0.0005). ConclusionOur findings showed that miR-26a might be involved in the pathogenesis of DVT. Additionally, measuring the expression of miR-26a could be used as a diagnostic or predictive biomarker in DVT.

Long non-coding RNA growth arrest specific 5 regulates the T helper 17/regulatory T balance by targeting miR-23a in myasthenia gravis.

ObjectiveMyasthenia gravis (MG) is a chronic autoimmune neuromuscular disorder. Recent studies report that long non-coding RNAs (lncRNAs) play vital roles in the pathogenesis of various diseases. This study explored the molecular mechanism of lncRNA growth arrest specific 5 (GAS5) in regulating the T helper 17 (Th17)/regulatory T (Treg) cell balance in MG.MethodsGAS5 and miR-23a expression levels were detected by quantitative reverse transcription polymerase chain reaction. Flow cytometry was performed to examine the proportion of Th17 and Treg cells in CD4+ T cells from MG patients. The interaction between GAS5 and miR-23a was verified by luciferase reporter and RNA immunoprecipitation assays. Levels of Th17 and Treg-related proteins were examined using western blots and enzyme-linked immunosorbent assays.ResultsGAS5 expression levels were significantly decreased in the CD4+ T cells of MG patients, and GAS5 overexpression restrained Th17 differentiation in CD4+ T cells. Moreover, miR-23a was confirmed as a downstream target of GAS5 and negatively regulated by GAS5 through a direct interaction. Further exploration showed that GAS5 can inhibit Th17 differentiation by downregulating miR-23a.ConclusionCollectively, our results indicate that GAS5 can regulate the Th17/Treg balance by targeting miR-23a expression, providing a scientific basis for clinical therapeutic development for MG.

MicroRNA-148a Inhibits Hepatocellular Carcinoma Cell Growth via Epithelial-to-Mesenchymal Transition and PI3K/AKT Signaling Pathways by Targeting Death Receptor-5.

The purpose of this study was to investigate the role of microRNA-148a (miR-148a) in hepatocellular carcinoma (HCC) metastasis and explore its potential mechanism in HCC cells. Expression levels of miR-148a were measured using qRT-PCR in 120 HCC tissue samples and two HCC cell lines. Migration and invasion assays were used to determine the role of miR-148a in HCC cells. Flow cytometry was used to access the effect of miR-148a on cell cycle of HCC cells. Western blot was performed to analyze the effect of miR-148a on epithelial-to-mesenchymal transition (EMT) and PI3K/AKT signaling pathways in HCC cells. Luciferase reporter assay was conducted to explore the downstream targets and biological function of miR-148a in HCC cells. The results showed that level of miR-148a was significantly downregulated in both HCC tissue and plasma samples in HCC patients. A higher level of miR-148a was positively correlated with better survival time and prognosis of HCC patients. Transfection of miR-148a inhibited the proliferation, migration and invasion of HCC cell lines. Transfection of miR-148a arrested HCC cells at S phase and promoted apoptosis of HCC cells. Death receptor-5 (DR-5) was identified as a direct target of miR-148a in HCC cell lines. Western blot and qRT-PCR analyses showed that miR-148a upregulated EMT and downregulated PI3K/AKT signaling pathways in HCC cell lines. In conclusion, data in the current study indicate that miR-148a inhibits HCC cells growth via downregulation of EMT and PI3K/AKT signaling pathways by targeting death receptor. These data suggest that miR-148a may serve as a therapeutic target for HCC cancer therapy in the future.

MiR-196a Upregulation Contributes to Gefitinib Resistance through Inhibiting GLTP Expression.

Tyrosine kinase inhibitor (TKI) therapy has greatly improved lung cancer survival in patients with epidermal growth factor receptor (EGFR) mutations. However, the development of TKI-acquired resistance is the major problem to be overcome. In this study, we found that miR-196a expression was greatly induced in gefitinib-resistant lung cancer cells. To understand the role and mechanism of miR-196a in TKI resistance, we found that miR-196a-forced expression alone increased cell resistance to gefitinib treatment in vitro and in vivo by inducing cell proliferation and inhibiting cell apoptosis. We identified the transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) bound to the promoter region of miR-196a and induced miR-196a expression at the transcriptional level. NRF2-forced expression also significantly increased expression levels of miR-196a, and was an upstream inducer of miR-196a to mediate gefitinib resistance. We also found that glycolipid transfer protein (GLTP) was a functional direct target of miR-196a, and downregulation of GLTP by miR-196a was responsible for gefitinib resistance. GLTP overexpression alone was sufficient to increase the sensitivity of lung cancer cells to gefitinib treatment. Our studies identified a new role and mechanism of NRF2/miR-196a/GLTP pathway in TKI resistance and lung tumor development, which may be used as a new biomarker (s) for TKI resistance or as a new therapeutic target in the future.

Research on Correlations of miR-196a Expression with Progression and Prognosis of Cutaneous Squamous Cell Carcinoma.

PurposeThis study aimed to investigate the correlation between miR-196a expression and the progression and prognosis of cutaneous squamous cell carcinoma (CSCC).Patients and MethodsTissue samples and corresponding paracancerous tissue samples from 117 patients with CSCC were collected. The qRT-PCR analysis was used to detect the expression levels of miR-196a. Kaplan–Meier curve and Cox regression analyses were used to analyze the relationship between miR-196a expression and patients’ prognosis. The CCK-8 and transwell assays were used to explore the effects of miR-196a on the abilities of cell proliferation, migration, or invasion.ResultsmiR-196a expression was significantly up-regulated in CSCC tissues or cell lines, compared with adjacent normal tissues or cell lines, respectively. High expression of miR-196a was associated with positive lymph node metastasis, high TNM stages, and a lower five-year survival rate. The expression level of miR-196a was up-regulated and the proliferation, migration or invasion ability of cells were significantly increased accordingly.ConclusionmiR-196a is highly expressed in CSCC, thus affecting the occurrence and development of CSCC. More importantly, miR-196a was shown to have potential as a prognostic marker for CSCC.

The role of miR-26a, miR-29a and miR-448-3p in the development of cerebral aneurysm.

Cerebral aneurysms cause the weakening and abnormal expansion of the arterial wall. MicroRNAs (miRNAs) are small noncoding RNAs of approximately 22 nucleotides in length that regulate gene expression. This study aimed to elucidate the role of miRNAs in the development of cerebral aneurysms. This study compared the expression levels of miR-26a, miR-29a and miR-448-3p in 50 samples each of cerebral aneurysm tissues and normal superficial temporal artery tissues. The miRNA expression levels were also compared in terms of aneurysm location and rupture status, i.e., presence or absence of rupture. Expression levels of miR-26a, miR-29a and miR-448-3p were increased in aneurysm tissues compared with normal vascular tissues. No significant difference was found in the miRNA expression levels with respect to aneurysm location or rupture status. This study showed that miR-26a, miR-29a and miR-448-3p overexpression could play an important role in intracranial aneurysm development independent of aneurysm location and rupture status. miR-26a, miR-29a and miR-448-3p could act as potential therapeutic targets in patients with intracranial aneurysms; however, further studies are needed on this issue.

In Vitro Investigations of miR-33a Expression in Estrogen Receptor-Targeting Therapies in Breast Cancer Cells.

Simple SummaryAltered metabolic pathways determine the aggressivity of breast cancer cells. To highlight the potential markers gains importance to understand early molecular signatures of disease. microRNAs are the small non-coding RNAs found in different biological samples. Due to the dysregulation of metabolic pathways, the expression and secretion of microRNAs are modulated.(1) Background: Increased fatty acid synthesis leads to the aggressive phenotype of breast cancer and renders efficiency of therapeutics. Regulatory microRNAs (miRNAs) on lipid biosynthesis pathways as miR-33a have potential to clarify the exact mechanism. (2) Methods: We determined miR-33a expression levels following exposure of MCF-7 and MDA-MB-231 breast cancer cells to estrogen receptor (ER) activator (estradiol-17β, E2) or anti-estrogens (ICI 182,780, Fulvestrant, FUL) at non-cytotoxic concentrations. We related miR-33a expression levels in the cells to cellular lipid biosynthesis-related pathways through immunoblotting. (3) Results: miR-33a mimic treatment led to significantly downregulation of fatty acid synthase (FASN) in MCF-7 cells but not in MDA-MB-231 cells in the presence of estradiol-17β (E2) or Fulvestrant (FUL). In contrast to the miR-33a inhibitor effect, miR-33a mimic co-transfection with E2 or FUL led to diminished AMP-activated protein kinase α (AMPKα) activity in MCF-7 cells. E2 increases FASN levels in MDA-MB-231 cells regardless of miR-33a cellular levels. miR-33a inhibitor co-treatment suppressed E2-mediated AMPKα activity in MDA-MB-231 cells. (4) Conclusions: The cellular expression levels of miR-33a are critical to understanding differential responses which include cellular energy sensors such as AMPKα activation status in breast cancer cells.

Correlation of circulating miRNA-33a and miRNA-122 with lipid metabolism among Egyptian patients with metabolic syndrome

BackgroundMetabolic syndrome is defined as a group of interrelated biochemical, clinical, and metabolic factors that directly increase the risk of cardiovascular disease, obesity, and type 2 diabetes mellitus. MicroRNA-33a (miR-33a) and MicroRNA-122 (miR-122) play a crucial role in various biological processes by regulating the gene expression level through post-transcriptional mechanisms, and alterations of their levels are associated with lipid and glucose metabolic disorders. In the present study, we aimed to investigate the correlation of miR-33a and miR-122 with obesity indices and glycemic parameters in a cohort of Egyptian patients. Quantitative real-time polymerase chain reaction (RT-PCR) using TaqMan assay was carried out to estimate the expression levels of miR-33a and miR-122 in serum samples of 100 patients diagnosed as having metabolic syndrome and 50 healthy controls. All patients (100%) had type 2 diabetes (by both history and laboratory assessment) and 70% were obese (BMI ≥ 30 kg/m2). ResultsCompared to controls, patients had significantly higher serum expression level of miR-33a (p value < 0.001) and miR-122 (p value = 0.0016). miR-33a was less expressed (downregulation expression) with 0.8 fold change in the patient group (obese and diabetic) compared to healthy controls, while miR-122 was highly expressed (upregulation expression) in the patient group of patients with 1.9 fold change. Clinical parameters as body mass index (BMI), wrist circumference (Wc), weight (Wt), and height (Ht) (all p < 0.001); total cholesterol (TC) (p = 0.0115); and triglyceride (TG) (p = 0.0286), all were significantly higher in patients compared to the healthy group. Both miRNAs show statistically significant correlations with clinical and biochemical parameters (p < 0.001). ConclusionsCirculating miR-33a and miR-122 might be convincing as possible biomarkers for the diagnosis of metabolic syndrome.

Circulating skeletal muscle related microRNAs profile in Piedmontese cattle during different age

Piedmontese cattle is known for double-muscle phenotype. MicroRNAs (miRNAs) play important role as regulators in skeletal muscle physiological processes, and we hypothesize that plasma miRNAs expression profiles could be affected by skeletal muscle growth status related to age. Plasma samples of cattle were collected during four different ages from first week of life until the time of commercial end of the fattening period before slaughter. Small-RNA sequencing data analysis revealed the presence of 40% of muscle-related miRNAs among the top 25 highly expressed miRNAs and, 19 miRNAs showed differential expression too. Using qRT-PCR, we validated in a larger bovine population, miRNAs involved in skeletal muscle physiology pathways. Comparing new-born with the other age groups, miR-10b, miR-126-5p, miR-143 and miR-146b were significantly up-regulated, whereas miR-21-5p, miR-221, miR-223 and miR-30b-5p were significantly down-regulated. High expression levels of miR-23a in all the groups were found. Myostatin, a negative regulator of skeletal muscle hypertrophy, was predicted as the target gene for miR-23a and miR-126-5p and we demonstrated their direct binding. Correlation analysis revealed association between miRNAs expression profiles and animals’ weights along the age. Circulating miRNAs could be promising for future studies on their biomarker potentialities to beef cattle selection.

Role of mir-33a, mir-203b, mir361-3p, and mir-424 in hepatocellular carcinoma

Background/aimHepatocellular carcinoma (HCC) is one of the most aggressive cancer types. MicroRNAs (miRNAs) are small noncoding regulatory RNAs that function posttranscriptionally. miRNA deregulation was observed in the development and progression of HCC. In this study, we aimed to investigate the expression levels of four miRNAs (mir-33a, mir-203b, mir361-3p, and mir-424) in HCC patients in comparison to healthy individuals.Materials and methodsVenous blood samples were collected from both HCC patients and healthy individuals. In order to determine the relative expression levels of mir-33a, mir-203b, mir361-3p, and hsa-mir-424 in HCC patients, probe-based quantitative real time PCR (qRT-PCR) was performed. The cycle threshold (Ct) results were analyzed according to the 2−∆∆Ct method and statistical analyses were performed by SPSS Statistics version 15 for Windows.ResultsqRT-PCR analysis revealed that the expression levels of mir-33a (fold change: 7.3 and P < 0.001), mir-203b (fold change: 4.6 and P < 0.001), and mir361-3p (fold change: 5.1 and P < 0.001)were downregulated compared to healthy individuals and mir-424 did not show any significant change between HCC patients and controls.ConclusionOur results indicated that mir-33a, mir-203b, and mir-361-3p may significantly contribute to tumor pathogenesis in HCC and have potential to be used as a noninvasive biomarker for cancer therapy.

MiR-23a-3p regulates the proliferation and apoptosis of human lens epithelial cells by targeting Bcl-2 in an in vitro model of cataracts.

Cataracts account for ~50% of the cases of blindness in individuals worldwide. The apoptosis of lens epithelial cells (LECs) occurs during the formation of cataracts, which is a non-congenital condition. Numerous microRNAs (miRs) have been reported to regulate apoptosis in LECs. For instance, miR-23a expression levels were shown to be upregulated in cataractous lenses; however, the function of miR-23a in cataracts remains undetermined. To establish an in vitro model of cataracts, human LECs, HLE-B3 cells, were induced with 200 µmol/l H2O2 for 24 h. HLE-B3 cells were transfected with the miR-negative control (NC) mimic, miR-23a-3p mimic, miR-NC inhibitor, miR-23a-3p inhibitor, small interfering RNA (siRNA) targeting BCL2 (siRNA-BCL2) and siRNA-NC. The expression levels of miR-23a-3p were detected using reverse transcription-quantitative PCR. The interaction between miR-23a-3p and the 3'-untranslated region (UTR) of the target mRNA BCL2 was predicted by TargetScan 7.1, and further validated using a dual luciferase reporter assay. The BCL2 protein expression levels were analyzed using western blotting, cell proliferation was determined using a CCK-8 assay and the levels of cell apoptosis were analyzed using flow cytometric analysis. The results of the present study revealed that the expression levels of miR-23a-3p were significantly upregulated, while the expression levels of BCL2 were significantly downregulated in H2O2-induced HLE-B3 cells compared to untreated control cells. BCL2 was shown to be a target of miR-23a-3p. The miR-23a-3p inhibitor subsequently attenuated H2O2-induced apoptosis and increased the proliferation of HLE-B3 cells, which was partially reversed by siRNA-BCL2. In conclusion, the findings of the current study suggested that the inhibition of miR-23a-3p may attenuate H2O2-induced cataract formation by targeting BCL2, thus providing a novel therapeutic target for the treatment of patients with cataracts in the clinic.

Evaluation of the Expression of Circulating miR-16 and miR-26a in the plasma of Gastric Cancer Patients in Guilan province, North of Iran

Background and Aims: Gastric cancer (GC) is a global health problem and the second deadly type of cancer worldwide with 1000 deaths per year. Poor prognosis in the early stages is one of the burdens in the treatment of GC. MicroRNAs are 18-22 nucleotide non-coding RNAs which play critical roles in the regulation of gene expression. Nowadays, miRNAs are widely known as non-invasive biomarkers for various kinds of cancers. This study aimed to evaluate the expression level of circulating miR-16 and miR-26a in GC patients and investigate the potential prognostic role of these miRNAs. Material and Methods: Initially, 20 plasma samples were obtained from pre-and post-operative GC patients, and the expression of miR-16 and -26a were compared with that of 20 healthy controls. The miRNAs expression was investigated using Real-Time quantitative PCR. The association between the expression levels of these miRNAs and clinicopathological features was also investigated in this study. Results: MiR-16 was down-regulated in GC patients; however, miR-26a expression revealed no significant difference between patients and controls in this regard. Furthermore, the expression of two miRNAs showed no association with the grade, TNM stage, and smoking status of the patients. Eventually, decreased expression of miR-16 was not correlated with the expression level of miR-26a. Conclusion: The downregulation of circulating miR-16 introduces this microRNA as a candidate biomarker for the non-invasive early prognosis of GC.

MiR-196a targeting LRIG3 promotes the proliferation and migration of cervical cancer cells

In recent years, studies have found that miR-RNA plays a role in cell proliferation, differentiation, apoptosis and metabolism. Among them, miR-196a is closely related to cervical cancer. Therefore, this experiment investigates the effect of mir-196a expression on cervical cancer cells and related mechanisms. The expression level of miR-196a in the cervical cancer cell line was assayed with the RT-PCR method, and liposome transfection was used to investigate its up-regulation or down-regulation in cervical cancer cells. The CCK-8 method and flow cytometry were used to measure cervical cancer cell proliferation and apoptosis, while the Transwell assay was used to determine cell migration and invasion of each transfection group. Bioinformatics was used to predict the target gene of miR-196a, which was verified using dual luciferase report experiment and Western blot, and miR-196a was further transfected with si-LRIG3 to detect its reversal effect on miR-196a regulation. Inhibition of the expression of miR-196a significantly reduced the proliferation, migration and invasion of cervical cancer cells, and promoted their apoptosis. Results from dual luciferase assay showed that miR-196a and LRIG3 had direct targeting effects. Cell proliferation, migration and invasion were enhanced by a reduction in the expression level of LRIG3 protein after miR-196a inhibitor cells were transfected with si-LRIG3. The expression of miR-196a is up-regulated in cervical cancer, and it promotes the growth of cervical cancer by its targeting effect on LRIG3 expression, resulting in enhancement of the proliferation, migration and invasion ability of cervical cancer cells, and inhibition of apoptosis.

Differentially expressed miR-152, a potential biomarker for in-stent restenosis (ISR) in peripheral blood mononuclear cells (PBMCs) of coronary artery disease (CAD) patients

Background and aimsIn-stent restenosis (ISR) remains the most daunting challenge of current treatments of coronary artery disease (CAD). MicroRNAs (miRNAs) are prominent regulators of key pathological processes leading to restenosis and used as diagnostic tools in different studies. miR-152 and miR-148a are implicated to contribute in the putative intracellular mechanisms of ISR. The aim of present study is to investigate the potential early-stage diagnostic role of miR-152 and miR-148a expression levels for ISR in peripheral blood mononuclear cells (PBMCs) of patients who underwent stent implantation. Methods and resultsThe miRNAs that are supposed to be involved in the ISR were nominated by bioinformatics approach mainly using miRWalk3. Then by quantitative real-time PCR, we determined the relative expression of miR-152 and miR-148a of PBMCs from ISR patients with their age/sex-matched controls. ResultsThe presence of ISR significantly coincided with a decrease in the relative expression of miR-152. The area under the curve (AUC) for miR-152 receiver operating characteristic (ROC) curve was 0.717 (95% CI; 0.60–0.83) with a sensitivity of 70% and a specificity of 67%, suggesting that the miRNA expression level might be employed to identify patients at risk of ISR. ConclusionsTo the best of our knowledge, this is the first work to show that the miR-152 expression level can possibly be applied to predict CAD patients at risk of ISR. The results suggest that the expression levels of miR-152 in PBMCs may serve as a biomarker for ISR. Our finding suggests the importance of miRNA levels in PBMCs as a novel biological tool to detect diseases in their early clinical stages.