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Low expression of Lnc-ENST00000535078 inhibits the migration, invasion, and enhances apoptosis of CTPE-induced malignantly transformed BEAS-2B cells.

Authors :
Lu, Ping
Yang, Liu
Lei, Yanting
Zhao, Yuezeng
Tang, Zhihao
Shang, Pingping
Zhou, Xiaolei
Wang, Pengpeng
Wang, Wei
Feng, Feifei
Zhang, Qiao
Source :
Toxicology Research; Aug2024, Vol. 13 Issue 4, p1-10, 10p
Publication Year :
2024

Abstract

Long non-coding RNA (LncRNA) plays an important role in malignant transformation of cells. This study aimed to explore the role of Lnc-ENST00000535078 in the malignant transformation of immortalized human bronchial epithelial cells (BEAS-2B) induced by coal tar pitch extract (CTPE). The malignant transformation model of BEAS-2B cells exposed to CTPE. Cell proliferation was examined by Cell counting kit-8 (CCK-8) assay. Colony formation assay was used to assess the colony of cells. Cell migration and invasion were detected by Transwell analysis. Cell cycle progression and apoptotic status were assessed by flow cytometry. Differentially expressed genes were screened by RNA sequencing. The results showed that Lnc-ENST00000535078 expression was highest in malignantly transformed BEAS-2B cells passaged to the 30th generation. Knockdown of Lnc-ENST00000535078 inhibited the migration, invasion and anti-apoptotic abilities of malignantly transformed BEAS-2B cells. Transcriptome analysis found 608 differential genes. CCND1 and FOS genes were screened out because of their levels were positive correlation with the expression of Lnc-ENST00000535078, which were consistent with the RNA sequencing results. In conclusion, Low expression of Lnc-ENST00000535078 inhibits the migration and invasion of malignant transformed BEAS-2B cells and promotes apoptosis in these cells. Lnc-ENST00000556926 might affect the malignant transformation of cells through the regulation of CCND1 and FOS. This study may provide a potential target for intervention in CTPE-induced lung cancer. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
2045452X
Volume :
13
Issue :
4
Database :
Complementary Index
Journal :
Toxicology Research
Publication Type :
Academic Journal
Accession number :
179421838
Full Text :
https://doi.org/10.1093/toxres/tfae121