Potency of BNT162b2 and mRNA-1273 vaccine-induced neutralizing antibodies against severe acute respiratory syndrome-CoV-2 variants of concern: A systematic review of in vitro studies.

BNT162b2 and mRNA-1273 are two types of mRNA-based vaccine platforms that have received emergency use authorization. The emergence of novel severe acute respiratory syndrome (SARS-CoV-2) variants has raised concerns of reduced sensitivity to neutralization by their elicited antibodies. We aimed to systematically review the most recent in vitro studies evaluating the effectiveness of BNT162b2 and mRNA-1273 induced neutralizing antibodies against SARS-CoV-2 variants of concern. We searched PubMed, Scopus, and Web of Science in addition to bioRxiv and medRxiv with terms including 'SARS-CoV-2', 'BNT162b2', 'mRNA-1273', and 'neutralizing antibody' up to June 29, 2021. A modified version of the Consolidated Standards of Reporting Trials (CONSORT) checklist was used for assessing included study quality. A total 36 in vitro studies meeting the eligibility criteria were included in this systematic review. B.1.1.7 (Alpha), B.1.351 (Beta), P.1 (Gamma), and B.1.617.2 (Delta) are four SARS-CoV-2 variants that have recently been identified as variants of concern. Included studies implemented different methods regarding pseudovirus or live virus neutralization assays for measuring neutralization titres against utilized viruses. After two dose vaccination by BNT162b2 or mRNA-1273, the B.1.351 variant had the least sensitivity to neutralizing antibodies, while B.1.1.7 variant had the most sensitivity; that is, it was better neutralized relative to the comparator strain. P.1 and B.1.617.2 variants had an intermediate level of impaired naturalization activity of antibodies elicited by prior vaccination. Our review suggests that immune sera derived from vaccinated individuals might show reduced protection of individuals immunized with mRNA vaccines against more recent SARS-CoV-2 variants of concern.

ABO blood groups and risk of human immunodeficiency virus infection: A systematic review and meta-analysis.

The last few decades have seen a pandemic of human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS), which continues to cause substantial morbidity and mortality. ABO blood groups are anthropological and genetic characteristics of a population whose associations with HIV infection are still controversial. This systematic review with meta-analysis was undertaken to investigate whether certain blood groups may have associations with HIV infection. PubMed, Scopus and Web of Science databases were systematically searched as of 6 September 2021. Grey literature was identified through screening Google Scholar, and reference lists of relevant studies. All observational studies providing data on ABO blood group distribution among HIV-infected and uninfected participants were included. Using a random effect model, risk ratios (RR) and 95% confidence intervals (CIs) were pooled to quantify this relationship. Fifty eligible studies with a total of 3,068,244 participants and 6508 HIV-infected cases were included. The overall analysis found that blood group AB increased the risk of HIV infection by 19% as compared with non-AB blood groups (RR = 1.19, 95% CI: 1.03-1.39, p = 0.02). Pooled estimates for other blood groups failed to reach statistical significance. Subgroup analyses identified a positive relationship between AB blood group and HIV infection within Asia, patient populations (as opposed to blood donors and general populations), studies with lower sample sizes, high-income countries and studies with a moderate quality score. The sequential omission and re-analysis of studies within sensitivity analyses produced no change in the overall pooled effect. In conclusion, this study identified that blood group AB carriers were more susceptible to HIV infection. Future investigations should be directed toward clarification of the exact role of ABO blood groups in HIV infection and the possible underlying mechanisms.

The cross-talk between leptin and circadian rhythm signaling proteins in physiological processes: a systematic review.

BACKGROUND: Today, modern lifestyles and disrupted sleep patterns cause circadian clock rhythm impairments that are associated with altered leptin levels, which subsequently affect a wide range of physiological processes and have significant health burdens on societies. Nevertheless, there has been no systematic review of circadian clock genes and proteins, leptin, and related signaling pathways. METHODS: Accordingly, we systematically reviewed circadian clock proteins, leptin, and molecular mechanisms between them by searching Pubmed, Scopus, ProQuest, Web of Sciences, and Google Scholar until September 2022. After considering the inclusion and exclusion criteria, 20 animal studies were selected. The risk of bias was assessed in each study. RESULTS: The results clarified the reciprocal interconnected relationship between circadian clock genes and leptin. Circadian clock genes regulate leptin expression and signaling via different mechanisms, such as CLOCK-BMAL1 heterodimers, which increase the expression of PPARs. PPARs induce the expression of C/EBPα, a key factor in upregulating leptin expression. CLOCK-BMAL1 also induces the expression of Per1 and Rev-erb genes. PER1 activates mTORC1 and mTORC1 enhances the expression of C/EBPα. In addition, REV-ERBs activate the leptin signaling pathway. Also, leptin controls the expression of circadian clock genes by triggering the AMPK and ERK/MAPK signaling pathways, which regulate the activity of PPARs. Moreover, the roles of these molecular mechanisms are elucidated in different physiological processes and organs. CONCLUSIONS: Crosstalk between circadian clock genes and leptin and their affecting elements should be considered in the selection of new therapeutic targets for related disorders, especially obesity and metabolic impairments.

Male-biased association of endothelial nitric oxide synthase Asp298Glu substitution (NOS3-c.894G/T) with asthma risk and severity.

OBJECTIVE: The nitric-oxide pathway plays a crucial role in the pathogeneses of asthma and NOS3-encoded endothelial nitric oxide synthase is one of the main components of the pathway. Variants of NOS3 are known to contribute to asthma development and pathophysiology. METHODS: We investigated the association of NOS3-c.894G/T (rs1799983) with asthma risk and severity by studying frequencies of its genotypes and alleles in 555 asthmatics (93 intermittent, 240 mild, 158 moderate, and 64 severe asthma cases) and 351 control participants using the PCR-FRLP method, logistic regression analysis and generalized ordered logit estimates. RESULTS: GT genotype (ORadj: 1.39; CI: 1.04-1.85; p = 0.026), dominant model GT + TT (ORadj: 1.41; CI: 1.07-1.87; p = 0.015), and T allele (ORadj: 1.32; CI: 1.05-1.67; p = 0.018) was associated with increased ORs in asthmatics. Also, the frequency of GT + TT (ORadj: 1.55; CI: 1.01-2.38; p = 0.044) was significantly higher in males. Furthermore, GT genotype (ORadj: 1.39; CI: 1.04-1.85; p = 0.024), GT + TT (ORadj: 1.42; CI: 1.07-1.87; p = 0.014), and T allele (ORadj: 1.32; CI: 1.05-1.66; p = 0.018) in total population and GT + TT (ORadj: 1.56; CI: 1.02-2.37; p = 0.04) in males were significantly associated with increased risk of severe, moderate, mild, intermittent asthma vs. controls. Also, GT genotype (ORadj: 1.39; CI: 1.02-1.91; p = 0.039) was significantly more frequent in severe, moderate grades vs. lower severity grades in the total population. Frequencies of GT genotype (ORadj: 1.77; CI: 1.05-3.00; p = 0.032) and GT + TT (ORadj: 1.74; CI: 1.04-2.90; p = 0.036) in total population and GT genotype (ORadj: 2.40; CI: 1.16-4.97; p = 0.018) and GT + TT (ORadj: 2.30; CI: 1.12-4.74; p = 0.023) in male subpopulation were significantly higher in severe cases compared to lower grades. CONCLUSIONS: NOS3-c.894G/T may be associated with asthma risk and its severer grades, with greater effects in men.

Female-biased association of NOS2-c.1823C>T (rs2297518) with co-susceptibility to metabolic syndrome and asthma.

The nitric oxide (NO) pathway contributes to the pathogeneses of metabolic syndrome (MetS) and asthma. NOS2 encodes inducible-NO synthase, which is an important enzyme of the pathway, and its variations could affect the risk of asthma and MetS and thereby co-susceptibility to them. This study aims to estimate the association of NOS2-c.1823C>T with risk of asthma, MetS, and asthma with MetS condition (ASMetS), and with asthma stages: intermittent, mild, moderate, and severe asthma. The study included asthmatics (n = 555), MetS (n = 334), and ASMetS cases (n = 232) and 351 controls, which were genotyped by the PCR-RFLP method. The T allele was significantly associated with an increased risk of asthma and MetS in the sample population and females. CT genotype and CT+TT model were significantly associated with increased risk of ASMetS in females. A significant association between CT genotype and increased risk of ASMetS in the sample population and females was found in ASMetS versus MetS. In the sample population and among females, the T allele was significantly associated with severe asthma. The rs2297518 single nucleotide polymorphism of NOS2 contributes to the risk of MetS, asthma, and co-susceptibility to them, and this contribution may be stronger in females compared to males.

Single-Center Experience of Pulmonary Endarterectomy for Chronic Thromboembolic Pulmonary Hypertension: The Results from the Tabriz University Medical Sciences (TUMS) CTEPH Program.

INTRODUCTION: Pulmonary endarterectomy (PEA) remains the preferred and potentially curative option for patients with chronic thromboembolic pulmonary hypertension (CTEPH). This study aimed to report the results of PEA for CTEPH in a tertiary center in Tabriz, Iran. METHODS: We analyzed the results of 42 CTEPH patients undergoing PEA, who were enrolled in the Tabriz University of Medical Sciences (TUMS-CTEPH) from January 2016 to October 2020. The main outcome measures included the New York Heart Association (NYHA) functional classification, the 6-Minute Walk Distance, hemodynamic measures in right heart catheterization, morbidity, and mortality. RESULTS: There was a significant improvement in the NYHA function class (2.6 ± 0.5 vs 1.1 ± 0.34), mean pulmonary arterial pressure (47.1 ± 13 vs 27.9 ± 8 mm Hg), cardiac output (4.3 ± 1.06 vs 5.9 ± 1.2 L/min), and pulmonary vascular resistance (709.4 ± 297.5 vs 214 ± 77 dyn s/cm5). Fifteen patients (35%) developed complications. The most common complication (10 [23%]) was reperfusion injury. Also, postsurgical mortality was 4% during hospital admission and 1-year follow-up. CONCLUSION: This is the first single-center report of PEA from Iran. Post-PEA and 1-year survival were acceptable as a referral center. PEA can be performed safe with low mortality. Greater awareness of PEA and patients' access to experienced CTEPH centers are important issues.

Long non-coding RNAs as potential biomarkers in the prognosis and diagnosis of lung cancer: A review and target analysis.

Long non-coding RNAs (lncRNA) have been emerged as a novel class of molecular regulators in cancer. They are dysregulated in many types of cancer; however, there is not enough knowledge available on their expression and functional profiles. Lung cancer is the leading cause of the cancer deaths worldwide. Generally, lncRNAs may be associated with lung tumor pathogenesis and they may act as biomarkers for the cancer prognosis and diagnosis. Compared to other invasive prognostic and diagnostic methods, detection of lncRNAs might be a user-friendly and noninvasive method. In this review article, we selected 27 tumor-associated lncRNAs by literature reviewing to further discussing in detail for using as diagnostic and prognostic biomarkers in lung cancer. Also, in an in silico target analysis, the "Experimentally supported functional regulation" approach of the LncTarD web tool was used to identifying the target genes and regulatory mechanisms of the selected lncRNAs. The reports on diagnostic and prognostic potential of all selected lncRNAs were discussed. However, the target genes and regulatory mechanisms of the 22 lncRNAs were identified by in silico analysis and we found the pathways that are controlled by each target group of lncRNAs. They use epigenetic mechanisms, ceRNA mechanisms, protein interaction and sponge mechanism. Also, 10, 23, 5, and 28 target genes for each of these mechanisms were identified, respectively. Finally, each group of target genes controls 50, 12, 7, and 2 molecular pathways, respectively. In conclusion, LncRNAs could be used as biomarkers in lung cancer due to their roles in control of several signaling pathways related to lung tumors. Also, it seems that lncRNAs, which use epigenetic mechanisms for modulating a large number of pathways, could be considered as important subjects for lung cancer-related diagnostic and prognostic biomarkers.

Comparison of losartan and amlodipine effects on the outcomes of patient with COVID-19 and primary hypertension: A randomised clinical trial.

BACKGROUND: Controversy exists regarding the drug selection in hypertension (HTN) management in patients with COVID-19. This study aimed to compare the effects of losartan and amlodipine in patients with primary HTN and COVID-19. METHODS: In this randomised clinical trial, hospitalised patients with COVID-19 and primary HTN were enrolled in the study. One arm received losartan, 25 mg, twice a day and the other arm received amlodipine, 5 mg per day for 2 weeks. The main outcomes were compare 30-day mortality rate and length of hospital stay. RESULTS: The mean age of patients treated with losartan (N = 41) and amlodipine (N = 39) was 67.3 ± 14.8 and 60.1 ± 17.3 years, respectively (P value = .068). The length of hospital stay in losartan and amlodipine groups was 4.57 ± 2.59 and 7.30 ± 8.70 days, respectively (P value = .085). Also, the length of ICU admission in losartan and amlodipine group was 7.13 ± 5.99 and 7.15 ± 9.95 days, respectively (P value = .994). The 30-day mortality was two and five patients in losartan and amlodipine groups, respectively (P value = .241). CONCLUSIONS: There was no priority in losartan or amlodipine administration in COVID-19 patients with primary HTN in decreasing mortality rate, hospital and ICU length stay. Further studies need to clarify the first-line anti-HTN medications in COVID-19.

Air pollution-related asthma profiles among children/adolescents: A multi-group latent class analysis.

BACKGROUND: This study aimed to investigate the asthma profile among children/adolescents and the relationship of the prevalence of air pollution profiles using latent class analysis (LCA). OBJECTIVES: In this cross-sectional study, a case rural community was selected in an industrial area, and two rural control communities were selected in unexposed areas. METHODS: Hourly concentrations of PM10, SO2, NO2, and total volatile organic compounds were obtained from the records of a fixed air quality monitoring station, and the concentrations of benzene, toluene, xylenes styrene were measured during six campaigns. Asthma data was collected using the International Study of Asthma and Allergies in Childhood in 7-18 years old children/adolescents. The modeling was conducted using LCA. RESULTS: A higher amount of air pollution indices were observed in the case than both control communities. LCA divided the participants into three clusters; "healthy" (92.8%), "moderate" (2.8%), and "severe" (4.4%). A higher probability of severe asthma (6.8%) was observed in the case than control communities (2.6% and 1.8%). Additionally, after adjusting for possible confounders, the odds of asthma was lower in the control communities than the case in both moderate and sever classes (Odds Ratios in the range of 0.135-0.697). CONCLUSIONS: This study indicates asthma profiles of children/adolescents and the higher prevalence of severe class in the area, explaining the possible effect of air pollution.

Comparison of spirometry and impulse oscillometry in methacholine challenge test for the detection of airway hyperresponsiveness in adults.

INTRODUCTION: Airway hyper-responsiveness (AHR) is a characteristic feature of asthma. The aim of this study was to compare the impulse oscillometry (IOS) and spirometry to methacholine for AHR detection among individuals with clinically hyper-reactive airway disease suggestive of bronchial asthma and baseline spirometry were normal. MATERIALS AND METHODS: Adults with symptoms suggestive of AHR and normal baseline spirometry test were selected. The short protocol of methacholine challenge test (MCT) was performed for all subjects using IOS and spirometry simultaneously. The primary endpoint was to compare the methacholine dosage causing a 20% drop in forced expiratory volume in one second (FEV1), with methacholine dosage that causing 40% increasing the baseline respiratory resistance at 5 hertz (R5), as measured by IOS. RESULT: A total of 235 participants were analyzed, 184 (78.2%) had positive test results with R5, while 81 (34.4%) had positive MCT results with FEV1.The sensitivity and specificity of MCT with R5were 87.3%, 64.6%, and MCT with FEV1 were 39.1%, 85.4%, respectively. The area under the receiver operating characteristic (ROC) curve was greater at lower doses of MCT at R5, (AUROC: 0.653; p= 0.01). CONCLUSIONS: The results showed higher sensitivity, negative predictive value, and earlier response of the short protocol of MCT with IOS, compared to MCT with spirometry. Our study suggested the utility of IOS in addition to conventional spirometry as a method of choice in MCT for detection of AHR.

Interleukin-17 mRNA expression and serum levels in Behçet's disease.

Behçet's disease (BD) was considered a T-helper 1 (Th1)-mediated autoimmune disease, but with the introduction of Th17 cells, their role in the pathogenesis of BD was also addressed. Despite studies on IL-17 in BD, the prognostic value of this cytokine in BD is unclear. The aim of this study is to determine the IL-17 mRNA expression rate and serum levels in patients with BD and its correlation with clinical manifestations and activity of BD. Forty-six BD patients in the active phase of the disease and 70 healthy controls were recruited in this study. BD activity was measured by Behçet's disease current activity form (BDCAF), Iranian Behçet's disease dynamic activity measure (IBDDAM) and total inflammatory activity index (TIAI). The IL-17 mRNA expression and serum levels were significantly higher in the BD patients compared with the healthy controls. These parameters in the BD patients aged <25 at disease onset, positive pathergy test, and positive HLA-B5 and HA-B51 were significantly higher than the healthy controls (P < 0.05). The IL-17 serum level in the patients with active uveitis was lower than the patients with in-active uveitis. There was no association between other clinical manifestations of BD and these parameters. No significant correlation was found between BDCAF and IBDDAM with IL-17 mRNA expression and serum levels. However, TIAI had a significant and negative correlation with the serum levels of IL-17.

Survivin modulatory role in autoimmune and autoinflammatory diseases.

Baculoviral IAP repeat containing 5 (BIRC5) gene encodes the important protein as survivin, a multifunctional protein, which is involved in cellular and molecular networks, progression of cell cycle, homeostasis, developmental morphogenesis, and apoptosis. The proximal BIRC5 promoter possesses specific binding sites for key transcription factors such as nuclear factor κB and signal transducer and activator of transcription 3. Upregulation of survivin exacerbates the autoimmune diseases (AIDs) including multiple sclerosis and myasthenia gravis by reducing the activity threshold of survivin-specific cytotoxic T cells. DNA damage along with upregulation or downregulation of survivin have been demonstrated in initiation and pathogenesis of cancers and AIDs. However, detailed mechanism of survivin function in pathogenesis of AIDs is not well understood. This review focuses on the structure, specificity, regulation, and function of survivin in physiologic conditions and pathogenesis of AIDs.

Combination therapy with KRAS siRNA and EGFR inhibitor AZD8931 suppresses lung cancer cell growth in vitro.

Lung cancer is a leading cause of cancer-related deaths worldwide, with less than a 5-year survival rate for both men and women. Epidermal growth factor receptor (EGFR) and Kirsten rat sarcoma oncogene (KRAS) signaling pathways play a critical role in the proliferation and progression of various cancers, including lung cancer. Genetic studies have shown that amplification, over-expression, or mutation of EGFR is an early and major molecular event in many human tumors. KRAS mutation is a negative factor in various cancer, including non-small-cell lung cancer, and complicates therapeutic approaches with adjuvant chemotherapy and anti-EGFR directed therapies. This article is dedicated to evaluating the synergistic effect of a novel EGFR inhibitor AZD8931 and KRAS small interfering RNA (siRNA) on the proliferation and apoptosis of lung adenocarcinoma cancer cells. A549 lung cancer cells were treated with KRAS siRNA and the EGFR inhibitor alone or in combination. The cytotoxic effects of KRAS siRNA and te EGFR inhibitor were determined usingMTT assay, and induction of apoptosis was determined by FACS analysis. Suppression of KRAS, Her-2, and EGFR expression by treatments was measured by qRT-PCR and western blotting. KRAS siRNA and the EGFR inhibitor significantly reduced the proliferation of A549 cells as well as KRAS and EGFR mRNA levels 24 hr after treatment. The results also indicated that the silencing of KRAS and EGFR has synergistic effects on the induction of apoptosis on the A549 cells. These results indicated that KRAS and EGFR might play important roles in the progression of lung cancer and could be potential therapeutic targets for treatment of lung cancer.

The relationship between microRNAs and Rab family GTPases in human cancers.

microRNAs (miRNAs), as a group of noncoding RNAs, posttranscriptionally control gene expression by binding to 3'-untranslated region (3'-UTR). Ras-associated binding (Rab) proteins function as molecular switches for regulating vesicular transport, which mainly have oncogenic roles in cancer development and preventing the efficacy of chemotherapies. Increased evidence supported that miRNAs/Rabs interaction have been determined as potential therapeutics for cancer therapy. Nevertheless, instability and cross-targeting of miRNAs are main limitations of using miRNA-based therapeutic. The mutual interplay between Rabs and miRNAs has been poorly understood. In the present review, we focused on the essence and activity of these molecules in cancer pathogenesis. Also, numerous hindrances and potential methods in the expansion of miRNA as an anticancer therapeutics are mentioned.

Diagnostic biomarker and therapeutic target applications of miR-326 in cancers: A systematic review.

MicroRNAs (miRNAs) are endogenous mediators of RNA interference and have key roles in the modulation of gene expression under healthy, inflamed, stimulated, carcinogenic, or other cells, and tissues of a pathological state. Many studies have proved the association between miRNAs and cancer. The role of miR-326 as a tumor suppressor miRNA in much human cancer confirmed. We will explain the history and the role of miRNAs changes, especially miR-326 in cancers and other pathological conditions. Attuned with these facts, this review highlights recent preclinical and clinical research performed on miRNAs as novel promising diagnostic biomarkers of patients at early stages, prediction of prognosis, and monitoring of the patients in response to treatment. All related publications retrieved from the PubMed database, with keywords such as epigenetic, miRNA, microRNA, miR-326, cancer, diagnostic biomarker, and therapeutic target similar terms from 1899 to 2018 with limitations in the English language. Recently, researchers have focused on the impacts of miRNAs and their association in inflammatory, autoinflammatory, and cancerous conditions. Recent studies have suggested a major pathogenic role in cancers and autoinflammatory diseases. Investigations have explained the role of miRNAs in cancers, autoimmunity, and autoinflammatory diseases, and so on. The miRNA-326 expression has an important role in cancer conditions and other diseases.

Targeting the KRAS, p38α, and NF-κB in lung adenocarcinoma cancer cells: The effect of combining RNA interferences with a chemical inhibitor.

BACKGROUND: Lung cancer is the leading cause of cancer-related death with less than 5-year survival rate for both men and women worldwide. KRAS (Kirsten rat sarcoma), nuclear factor-κB (NF-κB), and mitogen-activated protein kinase (MAPK) signaling pathways have a critical role in the proliferation and progression of various cancers, including lung cancer. The p38 MAPK plays a different role in various tissue hence show a tissue-dependent behavior. It acts as an oncogene in some tissues while plays as a tumor suppressor in some other tissues. Also, KRAS and NF-κB act as an oncogene in various cancer. This study was dedicated to analyzing the combined effect of NF-κB inhibitor, specific KRAS, and p38α small interfering RNA (siRNA) in A549 cell line. MATERIALS AND METHODS: The cytotoxic effects of p38α siRNA, KRAS siRNA, and NF-κB inhibitor were determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyl tetrazolium bromide (MTT) assay. Relative p38α, KRAS, and NF-κB messenger RNA (mRNA) levels were measured by quantitative reverse-transcription polymerase chain reaction. Induction of apoptosis by treatments was measured by fluorescence-activated cell sorting (FACS) analysis. RESULTS: The expression of mRNA related to p38α and KRAS genes was reduced to 23.4% and 26.7%, respectively, after treatment with specific siRNAs. Also, MTT assay showed that the cell viability after treatment with p38α siRNA, KRAS siRNA, NF-κB inhibitor and their combination was reduced. FACS results indicated that p38α siRNA, KRAS siRNA, and NF-κB inhibitor, and their combination, reduced the population of live cells in comparison with the population of untreated control cells (99.5%). The results are expressed as mean ± SD (n = 3); *P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001 vs control group. CONCLUSION: The results of this study indicated that p38α, KRAS, and NF-κB signaling pathways might play an important role in the development and growth of lung cancer and might be a potential therapeutic target for treatment of lung cancer.

The MicroRNA-326: Autoimmune diseases, diagnostic biomarker, and therapeutic target.

MicroRNAs (miRNAs) are uniquely regulated in healthy, inflamed, activated, cancerous, or other cells and tissues of a pathological state. Many studies confirm that immune dysregulation and autoimmune diseases with inflammation are correlated with various miRNA expression changes in targeted tissues and cells in innate or adaptive immunity. In this review, we will explain the history and classification of epigenetic changes. Next, we will describe the role of miRNAs changes, especially mir-326 in autoimmunity, autoinflammatory, and other pathological conditions. A systematic search of MEDLINE, Embase, and Cochrane Library was presented for all related studies from 1899 to 2017 with restrictions in the English language. In recent years, researchers have concentrated on mostly those roles of miRNA that are correlated with the inflammatory and anti-inflammatory process. Latest studies have proposed a fundamental pathogenic role in cancers and autoinflammatory diseases. Studies have described the role of microRNAs in autoimmunity and autoinflammatory diseases, cancers, and so on. The miRNA-326 expression plays a significant role in autoimmune and other types of diseases.

Potential Molecular Targets in the Treatment of Lung Cancer Using siRNA Technology.

Lung cancer is the leading cause of cancer-related mortality with about 1.6 million deaths every year worldwide. Gene mutations and overexpression of oncogenes play a central role in malignant transformation in NSCLC. Conventional approaches for treatments of NSCLC have shown low levels of success while showing severe side effects. Target therapy using siRNA has recently emerged as a new strategy for cancer treatment by specific targeting of genes involved in the development and metastasis of cancer. This article dedicated to an update review of molecular targets could potentially be used for target therapy of lung cancer using SiRNA technology.

A new insight on reciprocal relationship between microRNA expression and epigenetic modifications in human lung cancer.

Lung cancer stands among the leading causes of cancer-related death in the world. Although the molecular network implicated in lung cancer development is extensively revealed, the mortality rate is only slightly improved. MicroRNAs are small, endogenous single-stranded evolutionary conserved non-coding RNAs which involve in a wide variety of biological processes including cell growth, proliferation, metabolism, and differentiation. MicroRNAs, as novel biomarkers, have multiple functions in normal lung tissue development, and aberrant expression profiles of certain microRNAs could induce lung tumorigenesis. Similar to that of protein-coding genes, microRNA expression and function are regulated by multiple factors as well as the epigenetic network including DNA methylation and histone modification mechanisms. Furthermore, microRNAs can themselves regulate key enzymes which drive epigenetic modifications and have a pivotal effect on the cell biology. In this review, we will look into the regulatory loop linkage between microRNA expression and epigenetic modifications, and then, we will discuss the effects of epigenetics on the miRNome, as well as the role of epi-microRNAs in controlling the epigenome in human lung cancer. Better knowledge of reciprocal connection between microRNAs and epigenome will help to develop novel microRNA-orientated diagnostic, prognostic and therapeutic strategies related to human lung cancer in future.