Objectives: Tuberculosis (TB) remains a global public health problem. Recent studies have implicated long non-coding RNAs and their variants as possibly playing important roles in TB. The aim of this study was to assess the clinical relevance of lnc-AC145676.2.1-6 and lnc-TGS1-1 and their variants in a western Chinese population. Methods: This case-control study included 467 TB patients and 473 healthy controls from West China Hospital. The expression levels of lnc-AC145676.2.1-6 and lnc-TGS1-1 were analyzed by reverse transcriptase quantitative real-time PCR. Single-nucleotide polymorphism genotyping was performed using a custom-designed 2 Â 48-Plex SNPscan kit. Results: It was observed that lnc-AC145676.2.1-6 and lnc-TGS1-1 expression levels were both obviously down-regulated in TB patients. In addition, a lower expression level of lnc-TGS1-1 was associated with the presence of thrombocytopenia in TB patients during anti-TB treatment, and the homozygous CC genotype of rs4737420 correlated with a decreased risk of leukopenia, compared with individuals with the T allele (TT/CT genotype), in the dominant mode. Conclusions: For the first time, potential TB-associated promoting effects were identified for the decreased expression levels of lnc-AC145676.2.1-6 and lnc-TGS-1, while lnc-TGS1-1 and its variant rs4737420 may be predictive indicators of anti-TB drug-induced adverse drug reactions. Larger validation studies on different populations are warranted to confirm these findings.
Hepatocellular carcinoma (HCC, LIHC) is a kind of primary liver cancer with high mortality. 1 Genetic and epigenetic changes, chronic hepatitis B, hepatitis C virus infection, aflatoxin exposure, smoking, obesity, and diabetes are the main risk factors for HCC. 2 In recent years, many studies focused on the molecular pathogenesis of HCC and found a series of genetic and epigenetic events that promote the tumorigenesis and development of HCC. 3 Oxidative stress is usually increased in HCC, resulting in the increase of reactive oxygen species (ROS), then resulting in DNA damage, affecting the regulation of cell proliferation-related pathways, thus promoting the tumorigenesis and development of HCC. 4 The repair methods of DNA damage include mismatch repair, excision repair,
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