Differently expressed long noncoding RNAs and mRNAs in TK6 cells exposed to low dose hydroquinone

Abstract

Previous studies have shown that long noncoding RNAs (lncRNAs) were related to human carcinogenesis and might be designated as diagnosis and prognosis biomarkers. Hydroquinone (HQ), as one of the metabolites of benzene, was closely relevant to occupational benzene poisoning and occupational leukemia. Using high-throughput sequencing technology, we investigated differences in lncRNA and mRNA expression profiles between experimental group (HQ 20 μmol/L) and control group (PBS). Compared to control group, a total of 65 lncRNAs and 186 mRNAs were previously identified to be aberrantly expressed more than two fold change in experimental group. To validate the sequencing results, we selected 10 lncRNAs and 10 mRNAs for quantitative real-time PCR (qRT-PCR). Through GO annotation and KEGG pathway analysis, we obtained 3 mainly signaling pathways, including P53 signaling pathway, which plays an important role in tumorigenesis and progression. After that, 25 lncRNAs and 32 mRNAs formed the lncRNA-mRNA co-expression network were implemented to play biological functions of the dysregulated lncRNAs transcripts by regulating gene expression. The lncRNAs target genes prediction provided a new idea for the study of lncRNAs. Finally, we have another important discovery, which is screened out 11 new lncRNAs without annotated. All these results uncovered that lncRNA and mRNA expression profiles in TK6 cells exposed to low dose HQ were different from control group, helping to further study the toxicity mechanisms of HQ and providing a new direction for the therapy of leukemia.

Fabrication of an Extremely Cheap Poly(3,4-ethylenedioxythiophene) Modified Pencil Lead Electrode for Effective Hydroquinone Sensing

“…Hydroquinone (HQ) is considered one of the main benzene metabolites detected in human urine and blood, which could also be generated from chemicals of other sources, such as automobile exhaust, dietary intake, and cigarette smoke [ 1 , 2 , 3 , 4 , 5 , 6 , 7 ]. In humans, HQ is often found to form specific complexes with proteins that could interfere with the biological functions of proteins or induce the accumulation of oxidative stress that is inevitably responsible for DNA damage, apoptosis, cytotoxicity, and tumorigenesis [ 8 , 9 , 10 , 11 , 12 , 13 ]. Long-term exposure to HQ has been deliberated to play an important role in organ dysfunction, leukemia pathogenesis, and cancer formation [ 13 , 14 ].…”

“…In humans, HQ is often found to form specific complexes with proteins that could interfere with the biological functions of proteins or induce the accumulation of oxidative stress that is inevitably responsible for DNA damage, apoptosis, cytotoxicity, and tumorigenesis [ 8 , 9 , 10 , 11 , 12 , 13 ]. Long-term exposure to HQ has been deliberated to play an important role in organ dysfunction, leukemia pathogenesis, and cancer formation [ 13 , 14 ]. Therefore, tracing HQ in human urine and blood is strongly recommended in the pollution-intensive industrial society, especially for benzene-exposed workers.…”

Protective Effects of Aqueous Extracts of Flos lonicerae Japonicae against Hydroquinone‐Induced Toxicity in Hepatic L02 Cells

“…Hydroquinone (HQ) is a ubiquitous environmental chemical in cosmetics, medicines, the environment, and human diet; HQ can be metabolized from benzene as potentially hematotoxic, genotoxic, and carcinogenic compounds [1]. Humans are exposed to HQ through various channels, including oral administration, inhalation, and through the skin [2, 3].…”

“…Although the effects of HQ exposure on human health have been extensively studied and reported, the actual mechanisms of such effects remain unclear. The involved mechanisms trigger oxidative stress, which causes DNA damage, mutation in cellular transformation, in vivo tumorigenesis, gene toxicity, and epigenetic changes [1, 4–8]. In our previous experiments, HQ induced apoptosis in hepatic L02 cells by changing the cellular redox status by reducing the cellular thiol level and increasing the cellular reactive oxygen species (ROS) level.…”

“…In our previous experiments, HQ induced apoptosis in hepatic L02 cells by changing the cellular redox status by reducing the cellular thiol level and increasing the cellular reactive oxygen species (ROS) level. In addition, ROS can lead to DNA damage by breaking DNA or producing lipid peroxidation in the membrane, thereby increasing the degrees of apoptosis and necrosis of L02 hepatocytes [1, 9–11]. These findings indicated that HQ can damage L02 hepatocytes through a series of oxidative stress reactions, so it is possible to use some antioxidants for reducing HQ toxicity.…”