The activation of SIRT1 ameliorates BPDE-induced inflammatory damage in BEAS-2B cells via HMGB1/TLR4/NF-κB pathway.

Benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE), the metabolite of environmental pollutant benzo(a)pyrene (B(a)P) could induce pulmonary toxicity and inflammation. SIRT1, an NAD -dependent histone deacetylase, is known to regulate inflammation in the occurrence and development of various diseases, but its effects on BPDE-induced acute lung injury are still unknown. The present study aimed to explore the role of SIRT1 in BPDE-induced acute lung injury.

Endoplasmic reticulum stress regulates pyroptosis in BPDE-induced BEAS-2B cells.

Benzo(a)pyrene(B(a)P), as the main representative of polycyclic aromatic hydrocarbons, can promote inflammation and many chronic pulmonary diseases. However, the underlying mechanism of Benzo(a)pyrene-7,8-diol-9,10-epoxide (BPDE)-induced human bronchial epithelial cell pyroptosis related to endoplasmic reticulum stress (ERS) has not been elucidated. This study focused on the effects of BPDE on ERS and pyroptosis in human bronchial epithelial cells (BEAS-2B), and explored the relationship between ERS and pyroptosis.

Core genes in lung adenocarcinoma identified by integrated bioinformatic analysis.

This study aims to identify potential core genes of lung adenocarcinoma (LUAD). Three datasets (GSE32863, GSE43458, and GSE116959) were retrieved from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) between LUAD and normal tissues were filtrated by GEO2R tool.

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

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.

The relationship between endoplasmic reticulum stress and autophagy in apoptosis of BEAS-2B cells induced by cigarette smoke condensate.

Cigarette smoke (CS) is one of the severe risk factors for the development of the pulmonary disease. However, the underlying mechanisms, especially the CS-induced the human bronchial epithelial cells (BEAS-2B) apoptosis related to endoplasmic reticulum stress (ERS) and autophagy, remains to be studied. This study aims to investigate the relationship between ERS and autophagy in apoptosis induced by CS condensate (CSC).