BACKGROUND: LncRNA MEG3 rs7158663 has been shown to confer cancer susceptibility, maybe through altering its gene expression level. OBJECTIVE: We aimed to weigh the effect of rs7158663 on MEG3 serum level and breast cancer susceptibility. METHODS: We genotyped rs7158663 G > A and measured serum MEG3 in 150 breast cancer, 95 fibroadenoma , and 154 controls by the TaqMan method. RESULTS: The presence of rs7158663 G > A is a risk factor for breast cancer among fibroadenoma patients and controls, AA vs. GG genotypes (OR = 6.320, 95% CI = 2.587–15.439, 0.0001 when compared to controls and OR = 10.825, 95% CI = 1.929–60.742, P = 0.007 when compared to fibroadenoma). Decreased serum MEG3 was observed in breast cancer group when compared with fibroadenoma and/or controls [median (IQR) = 0.43 (0.27–0.55)] ( 0.0001). However, increased serum MEG3 was noted in fibroadenoma group when compared with controls ( 0.0001). A significance decreased serum MEG3 was found to be associated with mutant A allele than with wild G allele ( 0.0001). The results showed that rs7158663 and lower MEG3 were significantly associated with patients with higher TNM staging and larger tumor size > 5 cm. CONCLUSION: The presence of both rs7158663 and low MEG3 are diagnostic and unfavorable prognostic factors for BC patients.

Cerebrovascular stroke (CVS) is a potentially fatal disease. The most common risk factor for CVS is hypertension. While most studies in the field have focused on the functional roles of long noncoding RNAs (lncRNAs) NEAT1, GAS5, and HOTAIR in CVS, less attention has been paid to their clinical relevance to stroke incidence and prognosis. Also, a link has not yet been made between these lncRNAs and hypertension, our study aim was to investigate whether the expression of these lncRNAs differed between CVS with and without hypertension, as well as to compare each group to controls. In total, 181 CVS patients were enrolled, including 91 chronic hypertensive patients with stroke, 90 stroke patients without hypertension, and 51 control subjects. blood samples were collected on the day of recruitment from patients with CVS and controls. Real-time qRT-PCR was used to detect the expression of target lncRNAs in serum. When compared to controls, there was a statistically higher level of lncNEAT1 in each case group (median (IQR) = 3.68 (1.35–7.35) and 3.05 (0.95–6.45) for the hypertensive and non-hypertensive groups, respectively, with a significantly higher level in the hypertensive group (P = 0.04). When compared to controls, lncHOTAIR was significantly downregulated in all case groups (medians in hypertensive and non-hypertensive patients were 0.13, and 0.34, respectively), with a significantly lower level in the hypertensive group (P = 0.05). LncGAS5 levels in patients were significantly lower (median (IQR) = 0.16 (0.02–0.55) and 0.25 (0.03–0.99) for the hypertensive and non-hypertensive groups, respectively) compared to controls, with a significantly lower level in the hypertensive group (P = 0.02). There was a significant positive correlation between NEAT1 and GAS5, but a significant negative correlation between each with HOTAIR in both patients' groups. We also detected a significant negative correlation between each NEAT1 or GAS5 and NIHSS score while a significant positive correlation between HOTAIR and NIHSS. ROC curve analysis for GAS5 was able to differentiate patients with CVS hypertensive from patients with CVS non-hypertensive. Patients in each case group had statistically higher levels of NEAT1 and lower levels of HOTAIR and GAS5 compared to control levels, with higher significant NEAT1 but lower significant HOTAIR and GAS5 in the hypertensive group. Therefore, lncRNAs NEAT1, HOTAIR, and GAS5 could be used as diagnostic and prognostic biomarkers of CVS that correlate with NIHSS score and could produce a novel target for CVS therapy.

Systemic Lupus Erythematous (SLE) is a chronic systemic autoimmune disorder whose diagnosis depends on combination of multiple factors. Circulating lncRNAs could serve as diagnostic non-invasive bi...

Multiple sclerosis (MS) is an autoimmune disorder of the central nervous system. It was previously demonstrated that miR‑155 and miR‑146a served a vital role in the pathophysiology of MS, and single nucleotide polymorphisms in miR‑155 and miR‑146a were found to be associated with the susceptibility to different autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis and type I diabetes. The aim of the present study was to analyze the association between susceptibility to MS and two genetic polymorphisms (miR‑155 rs767649 A>T and miR‑146a rs57095329 A>G) in a cohort of Egyptian patients. The presence of the two polymorphisms were analyzed in 114 patients with MS and 152 healthy controls using quantitative PCR. The present study demonstrated for the first time that: The TT genotype and T allele in miR‑155 (rs767649 A>T) polymorphism were associated with an increased risk of MS; the miR‑146a (rs57095329 A>G) mutated G allele conferred protection against the development of MS in all genetic models; miR‑155 rs767649 A>T was a risk associated polymorphism of MS in females, but not in males; and miR‑155 rs767649 AT/TT and miR‑146a rs57095329 GG genotypes showed significantly higher distributions among patients with higher Expanded Disability Status Scale scores and secondary progressive MS subgroups. Therefore, miR‑155 rs767649 polymorphism may confer susceptibility to MS, whereas miR‑146a rs57095329 may be protective against MS in an Egyptian cohort.