Regulation of gene expression is essential for normal physiological functions; thus deregulation of gene expression is common in disease conditions. One level of regulation of gene expression is performed by noncoding RNAs, among which microRNAs (miRNA) are the best studied. Abnormal expression of these molecular players can lead to pathogenic processes such as heart disease, immune system abnormalities, and carcinogenesis, to name but a few. Of a length of 18–25 nucleotides miRNAs are involved in binding partial complementary sequences within the 3′-UTR (3′-untranslated region) of the target mRNAs. Depending on the type of neoplastic transformation, miRNAs can act both as oncogenes (oncomirs) or as tumor suppressors. Because of the great importance of miRNAs, most researches focus on either their role as biomarkers or their potential as therapeutic targets. Herein, we present the review of microRNA biology, function, and tumorigenic potential with emphasis on their role in lung cancer.

Background/Aim: Ovarian cancer is the most frequent cause of death in women among gynecological cancers in Poland. MMP-2 and MMP-9 are frequently dysregulated in cancers and they are considered as potential biomarkers. Our goal was to assess the associations between MMP-2 and MMP-9 mRNA expression, clinicopathological parameters and patients' response to chemotherapy. Materials and Methods: We evaluated MMP-2 and MMP-9 mRNA expression in epithelial ovarian cancer (EOC) tissues from 44 untreated patients, four ovarian cancer cell lines, and human skin fibroblasts (HSF). The expression of both MMPs was estimated using qPCR. Results: MMP-2 expression was significantly higher (p=0.020) in EOCs sensitive to chemotherapy compared to resistant and refractory tumors. The highest MMP-2 expression was found in HSF and MMP-9 expression was the highest in EOCs (p<0.001). The expression of neither MMP was significantly associated with patients' overall survival (OS). Conclusion: MMP-2 may be engaged in early stages of ovarian carcinogenesis. MMP-2 expression in EOCs may discriminate patients with a favorable response to first line chemotherapy.

Background: Numerous scientific studies on patients with autism spectrum disorder (ASD) suggest a significant role of inflammation processes or lipid disorders in this spectrum of neurodevelopmental disorders. Unfortunately, there is a lack of assessments of changes over time regarding level of lipids and inflammatory markers in people diagnosed with ASD using different diets. The aim of this study was to evaluate changes in lipid profile, high sensitivity C-reactive protein (hs-CRP) and body mass index (BMI) in individuals diagnosed with ASD and healthy controls. Variables were assessed at two time points (2015/17 and 2017/20) for each subject. Methods: After applying the selection criteria, for the first assessment period, 96 participants were qualified (the group consisted of 59 males with ASD and 37 healthy volunteers, i.e., age-matched control group—CG). The final assessment included 93 participants (57 from ASD group and 36 from CG). Subjects were on low-fat diet (LFD), gluten–casein-free diet (GF–CF) and regular diet (RD), respectively. All members of CG were on regular diet. A fasting lipid profile and hs-CRP level were analyzed. BMI and percentiles were calculated. Eating habits were checked by analyzing data from questionnaires. Principal component analysis (PCA) was used separately for every assessment. The Mann–Whitney U test was used to compare the medians of variables in the scheme of pairwise comparisons between control and ASD groups on different diets for separate assessment, while differences over time between variables were tested by Wilcoxon signed-rank test. Results: Statistically significant differences between BMI, CRP, triglycerides (TG), total cholesterol (TC), high-density lipoprotein (HDL), non-HDL-C and TC/HDL ratio were found in ASD group in comparison to healthy volunteers (increased BMI, CRP and TC/HDL and decreased HDL-C for all types of diets, increased TG in the group of LFD and RD individual and increased non-HDL-C in the group of GF–CF and RD individuals) during the first assessment period. The second assessment over time also showed increased levels of TC, non HDL-C and TC/HDL and decreased level of HDL-C for all ASD individuals regardless of diets used, while BMI and CRP increased only for individuals on LFD and RD. No statistically significant correlations between age of participants and other variables comparing with CG were found. Conclusions: Our studies suggest that targeted, individualized nutritional pattern and periodic screening for lipid and immune disorders would be beneficial for teenagers and adults diagnosed with ASD.

Lung cancer is a major cause of mortality worldwide and non-small cell lung cancer (NSCLC) accounts for over 80% of all cases of lung cancer. Despite efforts to develop and improve early screening methods, the majority of tumors are detected at advanced stages. For over 30 years, cisplatin (CDDP), or any of its analogues, has been used in the treatment of many types of tumors, including lung cancer. The use of platinum-based chemotherapeutics is limited by their toxicity and later on by the development of chemoresistance by tumor cells. The molecular mechanisms of CDDP resistance are not fully resolved. Genetic variants of DNA repair proteins, as well as proteins involved in drug accumulation or detoxification, play a crucial role in determining the cell's response to platinum-based chemotherapy. The identification of selected gene polymorphisms could improve the prognosis of a patient's response to therapy and overall survival. In this review we will focus on the gene polymorphisms involved in CDDP resistance, in particular in lung tumors, and discuss their potential as prognosis and survival markers.

Gestational diabetes mellitus (GDM) is a complex condition that involves a variety of pathological mechanisms, including pancreatic β-cell failure, insulin resistance, and inflammation. There is an increasing body of literature suggesting that these interrelated phenomena may arise from the common mechanism of endoplasmic reticulum (ER) stress. Both obesity-associated nutrient excess and hyperglycemia disturb ER function in protein folding and transport. This results in the accumulation of polypeptides in the ER lumen and impairs insulin secretion and signaling. Exercise elicits metabolic adaptive responses, which may help to restore normal chaperone expression in insulin-resistant tissues. Pharmacological induction of chaperones, mimicking the metabolic effect of exercise, is a promising therapeutic tool for preventing GDM by maintaining the body’s natural stress response. Metformin, a commonly used diabetes medication, has recently been identified as a modulator of ER-stress-associated inflammation. The results of recent studies suggest the potential use of chemical ER chaperones and antioxidant vitamins as therapeutic interventions that can prevent glucose-induced ER stress in GDM placentas. In this review, we discuss whether chaperones may significantly contribute to the pathogenesis of GDM, as well as whether they can be a potential therapeutic target in GDM treatment.