Effects of laparoscopic sleeve gastrectomy on serum lncRNA levels in obese patients

Obesity is a disease associated with excessive fat accumulation in the body, which body mass index (BMI) is greater than 30 kg/m. Bariatric surgery technique is one of the most common treatment options for obesity with the advantage of faster weight loss in a short time. lncRNAs play a role in adipogenesis and metabolic diseases, including obesity, type 2 diabetes, cardiovascular disease (CVD), osteoarthritis, and hypertension, so they are significant targets for therapeutic options. In this study, we aimed to determine lncRNAs and specific parameters that show different expressions in the plasma of patients with obesity. We included fifteen patients with BMI greater than 30 kg/m2 before and less than 30 kg/m2 after laparoscopic sleeve gastrectomy (LSG) in the study. Total RNAs, including lncRNAs and other non-coding RNAs, were isolated from plasma samples of patients, and eight lncRNAs (H19, Neat1, HOTAIR, ANRIL,  MALAT1, ATB, SNGH5, UCA1) were quantified by real-time PCR. Gene Ontology, KEGG, and relation of obesity analysis were utilized. Unpaired Student's t-test Pearson correlation analysis was used for statistical analysis. We observed a statistically significant increase in the expression levels of all lncRNAs in the patients with the post-operative BMI change. We have added a new dimension to the biomarker studies related to obesity and the clinical follow-up of patients undergoing LSG surgery. Further studies are required for enlighting the molecular mechanisms

Tumour suppressor PTEN enhanced enzyme activity of GPx, SOD and catalase by suppression of PI3K/AKT pathway in non-small cell lung cancer cell lines

Phosphates and tensin homologue deleted on chromosome 10 (PTEN) is a tumour suppressor gene which dephosphorilates phosphoinositol 3,4,5 triphosphates. Therefore PTEN can regulate PI3K/AKT pathway in cells. Because of promoter methylation or gene deletion, PTEN expression is commonly decreased or lost in non-small cell lung cancer (NSCLC) cell lines. Therefore, we hypothesized that PTEN could regulate the activity of superoxide dismutase (CuZnSOD), glutathione peroxidase (GPx) and catalase. We first recreated PTENwt, G129R and G129E expressions in lung cell lines, in which endogenous PTEN expression was not detected. Then, we showed that PTEN could suppress AKT activity by its lipid phosphatase domain. We then examined the effect of recreated PTEN expressions in NSCLC cells. While PTENwt expression caused enhanced activity of SOD, GPx and catalase in transfected cells lines, neither G129R nor G129E expression effected enzyme activities. These results suggest that PTEN can up-regulate SOD, GPx and catalase activity by inhibition of PI3K/AKT pathway in NSCLC cell lines. © 2013 Informa UK, Ltd

MYC-driven regulation of long non-coding RNA profiles in breast cancer cells.

AIM: MYC deregulation contributes to breast cancer development and progression. Deregulated expression levels of long non-coding RNAs (lncRNA) have been demonstrated to be critical players in development and/or maintenance of breast cancer. In this study we aimed to evaluate lncRNA expressions depending on MYC overexpression and knockdown in breast cancer cells. MATERIALS AND METHODS: Cells were infected with lentiviral vectors by either knockdown or overexpression of c-MYC. LncRNA cDNA was transcribed from total RNA samples and lncRNAs were evaluated by qRT-PCR. RESULTS: Our results indicated that some of the lncRNAs having tumor suppressor (GAS5, MEG3, lincRNA-p21) and oncogenic roles (HOTAIR) are regulated by c-MYC. CONCLUSION: We observed that c-MYC regulates lncRNAs that have important roles on proliferation, cell cycle and etc. Further studies will give us a light to identify molecular mechanisms related to MYC-lncRNA regulatory pathways in breast cancer

Design of a Lentiviral Vector for the Inducible Expression of MYC: A New Strategy for Construction Approach

Lentiviral vectors are powerful tools for gene expression studies. Here we report the construction of pTIJ, a vector for inducible gene expression. pTIJ was generated from pTRIPZ backbone, which is designed for the inducible expression of shRNA sequences, by the introducing of a multiple cloning site upstream of the Tet promoter and the removal of miR30 flanking sequences. To evaluate pTIJ as a tool for the inducible expression of genes of interest, we introduced MYC cDNA into pTIJ and infected two small cell lung cancer cell lines, H209 and H345. Induction of MYC expression by doxycycline was detectable in both cell lines by real-time PCR and western blot analysis. This study highlights the relevance of pTIJ vector to allow the inducible expression of any gene of interest. In our belief, pTIJ will be an extremely useful tool to simplify the generation of genetically engineered cell lines for the inducible expression of cDNA sequences in biological studies. Furthermore, we report the generation of a pTIJ-MYC vector for the inducible expression of the oncogene MYC. © 2017, Springer Science+Business Media New York

The effects of pulsed magnetic field on the key elements responsible for synthesis and destruction of elastin-collagen in diabetic lung tissue

Changes in the expression levels of genes responsible for synthesis-destruction of elastin-collagen and the occurrence of lung diseases are in correlation. Although, diabetes-related complications are important health problems, the mechanism by which diabetes exerts this effect is unclear. On the other hand, although the effect of pulsed magnetic field (PMF) in lung diseases has been shown, its mechanism of action is unknown. The study aimed to determine the effects of PMF on the key regulator elements of the synthesis-destruction of elastin-collagen at the transcriptional level. Rats were divided into groups as control, control + PMF 10Hz, diabetes, diabetes + PMF 10Hz. PMF groups were exposed to 10 Hz PMF for four weeks. In diabetic conditions, ELN, ELANE, and COL1A1 genes were dysregulated at the transcriptional level as their levels were 14.23±2.56; 7.62±1.37 and 0.24±0.04, respectively. Dysregulated ELN gene expressions were decreased to 6.17±1.97 by PMF application. There were no meaningful changes in gene expressions in control + PMF 10 Hz groups. The present study shows that ELN, ELANE, and COL1A1 may play a key role at the transcriptional level in the mechanism of diabetic-lung diseases. In addition, it may be said that "PMF shows its effect by re-regulating the expression level of ELN gene in diabetic lung tissues". In future studies, ELN gene-targeted PMF application methods may be developed. Moreover, PMF application might not affect the genes that are responsible for elastin-collagen synthesis-destruction in healthy lungs when the PMF is applied on different tissues for the treatment of various diseases. [Med-Science 2022; 11(2.000): 586-92