Lu Ping, Yang Liu, Lei Yanting, Zhao Yuezeng, Tang Zhihao, Shang Pingping, Zhou Xiaolei, Wang Pengpeng, Wang Wei, Feng Feifei, Zhang Qiao
Department of Toxicology, Zhengzhou University School of Public Health, Zhengzhou, Henan Province 450001, China.
Qinhuangdao Center for Disease Control and Prevention, Qinhuangdao, Hebei Province 066000, China.
Toxicol Res (Camb). 2024 Aug 21;13(4):tfae121. doi: 10.1093/toxres/tfae121. eCollection 2024 Aug.
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.
长链非编码RNA(LncRNA)在细胞恶性转化中起重要作用。本研究旨在探讨Lnc-ENST00000535078在煤焦油沥青提取物(CTPE)诱导的永生化人支气管上皮细胞(BEAS-2B)恶性转化中的作用。建立了暴露于CTPE的BEAS-2B细胞恶性转化模型。采用细胞计数试剂盒-8(CCK-8)法检测细胞增殖。集落形成试验用于评估细胞集落。通过Transwell分析检测细胞迁移和侵袭。采用流式细胞术评估细胞周期进程和凋亡状态。通过RNA测序筛选差异表达基因。结果显示,在传至第30代的恶性转化BEAS-2B细胞中,Lnc-ENST00000535078表达最高。敲低Lnc-ENST00000535078可抑制恶性转化BEAS-2B细胞的迁移、侵袭和抗凋亡能力。转录组分析发现608个差异基因。筛选出CCND1和FOS基因,因为它们的水平与Lnc-ENST00000535078的表达呈正相关,这与RNA测序结果一致。总之,Lnc-ENST00000535078低表达抑制恶性转化BEAS-2B细胞的迁移和侵袭,并促进这些细胞的凋亡。Lnc-ENST00000556926可能通过调控CCND1和FOS影响细胞的恶性转化。本研究可能为干预CTPE诱导的肺癌提供潜在靶点。