Skip to content


  • Poster presentation
  • Open Access

LncRNAs expression signatures of cadmium-induced malignant transformation of human bronchial epithelial cells revealed by microarray

  • 1,
  • 2,
  • 1,
  • 1 and
  • 1
Epigenetics & Chromatin20136 (Suppl 1) :P90

  • Published:


  • Gene Expression
  • Cadmium
  • Gene Function
  • Biological Function
  • 35th Cell


Cadmium (Cd) and its compounds are well-known environmental carcinogens, but the mechanisms underlying the carcinogenesis are not entirely understood yet. Long noncoding RNAs (IncRNAs) are an important class of pervasive genes involved in a variety of biological functions. They are aberrantly expressed in many types of cancers. In this study, we described IncRNAs profiles in 35th passage of CdCI2 malignant transformation cells(35th cell) and untransformed human bronchial epithelial cells(16HBE) by microarray.

Methodology/principal findings

With abundant and varied probes accounting 33,045 LncRNAs in our microarray, the number of IncRNAs that expressed at a certain level could be detected is 21409. From the data we found there were 369 IncRNAs were upregulated and 90 IncRNAs were downregulated (≥2.0fold-change, P<0.05) in 35th cells compared with 16HBE cells. Our data showed that upregulated IncRNAs were more common than downregulated ones. ENST00000477387, ENST00000394732, ENST00000485873, ENST00000497538, uc002odz.1, AK023660, NR_023938, BC019085 were evaluated by qPCR in 35th cells compared with 16HBE cells. The eigth IncRNAs were aberrantly expressed in 35th cells compared with matched 16HBE cells.


Our study is the first one to determine genome-wide IncRNAs expression patterns in Cadmium-induced malignant transformation by microarray. The results displayed that clusters of IncRNAs were aberrantly expressed in CdCI2 malignant transformation cells compared with 16HBE cells, which revealed that IncRNAs differentially expressed in CdCI2 malignant transformation cells may exert a partial or key role in cadmium-induced cancers. Taken together, this study may provide a viable mechanism for cadmium-induced cancers.

Authors’ Affiliations

School of public health, Guangzhou Medical University, Guangzhou, 510182, People’s Republic of China
Department of Internal Medicine of the First Hospital of Guangzhou, Guangzhou, 510180, China


© Zhou et al; licensee BioMed Central Ltd. 2013

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.