Expression of miR-9 and miR-200c, ZEB1, ZEB2 and E-cadherin in Non-Small Cell Lung Cancers in Iran

Document Type : Research Articles


1 Department of Molecular Medicine, Biotechnology Research center, Pasteur Institute of Iran, Tehran, Iran.

2 Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.

3 Tracheal Diseases Research Center (TDRC), National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran.

4 Department of Clinical Oncology, Queen Elizabeth Hospital, Kowloon, Hong Kong, China.


MicroRNAs (miRNAs) exert a critical influence on physiological and pathological processes through posttranscriptional
modification of their mRNA targets. They play important roles in tumorigenesis and are considered to
be potential diagnostic and prognostic biomarkers with various cancers. MiR-200c and miR-9 are regulatory elements
that can have dual impacts as oncogenes and/or tumor suppressor genes. MiR-200c regulates two transcription factors,
ZEB1 and ZEB2, while miR-9 is a regulatory factor for the E-cadherin protein which has a critical function in cell-cell
junctions and is inhibited by two transcription factors ZEB1 and ZEB2. In this study, expression levels of miR-200c
and miR-9, ZEB-1, ZEB-2 and E-cadherin were assessed in 30 non-small cell lung cancers (NSCLCs) by real-time
qPCR. MiR-9 was down-regulated significantly in tumor tissues compared to normal adjacent tissues, while there was
no significant change in expression level of miR-200c. On the other hand, ZEB1 demonstrated significant increase
and ZEB2a decrease at the mRNA level. These results indicate roles for miR-9 and ZEB1 in genesis of lung cancer,
although clinico-pathological associations were not evident. Further studies are necessary to assess implications for
treatment of lung cancer.


Main Subjects

Volume 20, Issue 6
June 2019
Pages 1633-1639
  • Receive Date: 22 December 2017
  • Revise Date: 21 October 2018
  • Accept Date: 06 January 2019
  • First Publish Date: 01 June 2019