LncRNA-ENST00000556926 regulates the proliferation, apoptosis and mRNA transcriptome of malignant-transformed BEAS-2B cells induced by coal tar pitch

Abstract

Abstract As a byproduct of coal tar distillation, coal tar pitch (CTP) has been proven to be carcinogenic to human. However, the mechanisms of lung cancer induced by CTP are still unclear. It has been shown that long non-coding RNAs (LncRNAs) play an important role in the development of human cancers. This study aims to investigate the effect of LncRNA-ENST00000556926 on malignant-transformed human bronchial epithelial (BAES-2B) cells induced by coal tar pitch extracts (CTPE). In this study, BEAS-2B cells were treated with 2.4 μg/ml of CTPE for 72 h and then passaged; and the cells were treated 4 times in the same procedure, then passaged until passage 30 (CTPE30). Cell counting kit-8 (CCK-8) assay was used to detect cell viability, then cell cycle and apoptosis were analyzed by flow cytometry, and transcriptome sequencing analysis was used to detect differentially expressed mRNAs after interference of ENST00000556926. The results indicated that the expression of ENST00000556926 in CTPE30 group was significantly higher compared with control group. Furthermore, after interfering the expression of ENST00000556926, cell viability was inhibited, and cell cycle was arrested while apoptosis of malignant-transformed BEAS-2B cells was promoted. Moreover, a total of 159 differentially expressed mRNAs were screened out after interference of ENST00000556926, including 62 up-regulated mRNAs and 97 down-regulated mRNAs. In addition, knockdown of ENST00000556926 decreased the expression of thioredoxin domain containing 5 (TXNDC5) and FOXD1. In conclusion, LncRNA-ENST00000556926 could regulate the proliferation, apoptosis and mRNA transcriptome of malignant-transformed BEAS-2B cells induced by CTP, which may provide a novel treatment strategy for lung cancer.