Roles of non-coding RNAs in cell death pathways involved in the treatment of resistance and recurrence of cancer.

Considering the burden of cancer, a number of methods have been applied to control or stop it. However, because of drug resistance or cancer recurrence, these treatments usually face failure. Combination of modulation of expression of non-coding RNAs (ncRNAs) with other treatments can increase treatment-sensitivity of tumors but these approaches still face some challenges. Gathering information in this field is a prerequisite to find more efficient cures for cancer. Cancer cells use ncRNAs to enhance uncontrolled proliferation originated from inactivation of cell death routs. In this review article, the main routes of cell death and involved ncRNAs in these routes are discussed. Moreover, extant information in the role of different ncRNAs on cell death pathways involved in the treatment resistance and cancer recurrence is summarized.

Interplay between fatty acid desaturase2 (FADS2) rs174583 genetic variant and dietary antioxidant capacity: cardio-metabolic risk factors in obese individuals.

OBJECTIVE: Polymorphisms of the fatty acid desaturase (FADS) gene cluster have been associated with obesity and its-related consequences. This cross-sectional study aimed to investigate whether the adherence to dietary non-enzymatic antioxidant capacity (NEAC), reflecting the antioxidant potential of the whole diet, modifies the association of FADS2 rs174583 polymorphism with cardio-metabolic risk factors in obese adults. METHODS: The present study included 347 healthy obese adults (aged 20-50 years). Dietary NEAC was assessed by a validated food frequency questionnaire with 147 items and estimated through total radical-trapping antioxidant parameters (TRAP), oxygen radical absorbance capacity (ORAC), and ferric reducing ability of plasma (FRAP) with the use of published databases. FADS2 rs174583 polymorphism was characterized using PCR-RFLP. ANCOVA multivariate interaction model was used to analyze gene-diet interactions. RESULTS: after adjustment for the confounding variables (age, physical activity, SES and WC), this study showed significant interactions between rs174583 polymorphism and adherence to dietary ORAC on the serum cholesterol (P Interaction = 0.029), LDL-C (P Interaction = 0.025) and HDL-C levels (P Interaction = 0.049) among the male group; minor allele carriers who had the highest adherence to the NEAC (ORAC) showed a better metabolic profile (lower TG and LDL-C and higher HDL-C) (P < 0.05). Among women, the dietary ORAC-rs174583 interactions were statistically significant for the serum insulin concentration (P Interaction = 0.020), QUICKI (P Interaction = 0.023) and HOMA-IR (P Interaction = 0.017); the highest QUICKI and the lowest HOMA-IR and serum insulin levels were observed in the CC homozygote carriers with the moderate compliance with the dietary ORAC (P < 0.05). In addition, the dietary TRAP modified the association between FADS2 variant and change in LDL-C levels (P Interaction = 0.037); the homozygous wild-type (CC) women who placed in the top tertile of TRAP had significantly the lowest LDL-C levels than those in the second tertile (P < 0.05). CONCLUSION: These data indicate that the FADS2 rs174583 polymorphism interacts with the dietary NEAC to influence cardio-metabolic risk factors in obese subjects. Replication in prospective cohort studies among other populations is required to confirm the results of our study.