Abstract

Objective:Recent studies have shown the role of autophagy in different types of cancer including lung cancer. MicroRNAs are considered as key factors in regulation of autophagy related genes. miR-30d, miR-204-5p and miR-20a are regulatory markers which can suppress the expression of beclin1, LC3, bcl2 and ULK1 as their target genes and they lead to decrement of autophagy in human cancer cells. Moreover, epigenetic modifications DNA methylation has been indicated in regulation of autophagy in different stages of cancer. Methods:In this study, the expression levels of miR-30d, miR-204-5p and miR-20a as well as their target genes were analyzed in 30 non-small cell lung cancers (NSCLCs) patients sample and adjacent normal tissues by real-time qPCR. In addition, DNA methylation of beclin1, LC3, bcl2 and ULK1 genes were assessed by MS-HRM method. Results: MiR-30d (p value= 0.01) and miR-204-5p (P=0.048) significantly down-regulated in tumor samples compared to normal adjacent tissues, while there was no significant change in expression level of miR-20a. On the other hand, target genes expression level was significantly increased in NSCLC tissues, however methylation pattern of the target gene promoters, did not show any significant alteration. Conclusion:These results indicate roles for miR-30d, miR-204-5p as tumor suppressor genes as well as target genes as oncogenes in NSCLC patients. Although these factors may have a significant role in NSCLC progression, further studies are necessary to investigate the implications of these findings for treatment of lung cancer.

Highlights

  • Lung cancer is the leading cause of cancer related death worldwide

  • MiR-30d and miR-204-5p expression were significantly decreased in non-small cell lung cancers (NSCLCs) patients, changes in the expression pattern of miR-20a in NSCLC samples compared to normal tissues has not been significant

  • According to some previous studies, miR-30d is found to be capable of suppressing NSCLC cell growth (Tang et al, 2019), this miRNA can act as a tumor suppressor in NSCLC

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Summary

Introduction

Lung cancer is the leading cause of cancer related death worldwide. Non-small cell lung cancer (NSCLC) accounts for approximately 85% of all lung cancer cases. Macro-autophagy (hereafter referred to as autophagy), which is a homeostatic mechanism regulating degradation of proteins, organelles, and other cellular components in lysosomes, plays an important role in cancer initiation, progression and development (Frankel and Lund, 2012). It is an evolutionary conserved phenomenon observed in all eukaryotic cells, from yeast to mammals involving in turnover of proteins and organelles as well as adaptation and survival, or death in different environmental unfavorable conditions such as nutrient deprivation and pathogen infection (Kondo et al, 2005). Malfunction of this catabolic pathway contributes to various human diseases including cancer (Frankel et al, 2011)

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