Lipopolysaccharide (LPS), the major outer surface membrane component of Gram-negative bacteria, is one of the main etiological factors in the pathogenesis of several lung diseases, such as chronic obstructive pulmonary disease. The respiratory epithelium and the macrophages comprise the dynamic interface between the outside environment and the host response to bacterial infection via cytokine secretion. In the present study, the mechanisms of LPS induced‑inflammatory response in human lung cells and macrophages were investigated. The effects of LPS exposure on cytokine production, inflammation‑related transcription factors and intracellular signaling pathway activation were assessed in human lung mucoepidermoid carcinoma H292 cells and human macrophage THP‑1 cells. The results demonstrated that LPS markedly increased the expression of interleukin (IL)‑6, IL‑8, tumor necrosis factor (TNF)‑α, matrix metallopeptidase (MMP)‑9 and tissue inhibitor of metalloproteinases‑1 in H292 cells, while it increased the production of IL‑6, IL‑8 and TNF‑α in differentiated THP‑1 cells. In addition, LPS exposure activated nuclear factor (NF)‑κB and activator protein (AP)‑1 signaling in H292 cells, while it activated NF‑κB and signal transducer and activator of transcription (STAT) 3 signaling in THP‑1 cells. Furthermore, treatment with NF‑κB, AP‑1 or STAT3 inhibitors significantly decreased the LPS‑mediated expression of IL‑8 and TNF‑α in these cells, suggesting that these pathways might serve crucial roles in LPS‑induced cytokine expression. In conclusion, LPS stimulation of H292 and THP‑1 cells induced cytokine expression and NF‑κB, mitogen‑activated protein kinase and Janus kinase/STAT3 pathway activation with subsequent nuclear translocation of NF‑κB, AP‑1 and STAT3, which demonstrated potential of the use of NF‑κB, AP‑1 and STAT3 in therapies for conditions and diseases associated with chronic inflammation.
Circular RNAs (circRNA), a class of noncoding RNAs, have been found to be involved in various diseases. Here, the expression levels of the circRNA hsa_circ_0001445 in 73 pairs of hepatocellular carcinoma (HCC) and adjacent nontumor tissues were investigated by quantitative real-time polymerase chain reaction (qRT-PCR). Our data demonstrate that the hsa_circ_0001445 levels were significantly decreased in HCC tissues (P < 0.001) and markedly associated with the number of tumor foci (P = 0.014). Furthermore, in vitro approaches showed that overexpression of hsa_circ_0001445 promoted apoptosis and inhibited proliferation, migration, and invasion of HCC-derived cells, suggesting that hsa_circ_0001445 might be involved in the development of HCC. In addition, we found that the plasma hsa_circ_0001445 transcription levels in HCC patients were lower than those in cirrhosis (P < 0.001) and hepatitis B (P < 0.001) patients as well as in healthy controls (P < 0.001). In fact, receiver operating characteristic curve analysis indicated that plasma hsa_circ_0001445 could be a fairly accurate marker to distinguish HCC cases from healthy controls as well as patients with cirrhosis or hepatitis B.
Long noncoding RNA (LncRNA) homeotic genes (HOX) transcript antisense RNA (HOTAIR) has been reported to play a vital role in various cancers. It has been found that HOTAIR was upregulated in non–small cell lung cancer (NSCLC) and involved in cell invasion and metastasis. The aberrant expression of HOTAIR is expected to serve as a potential biomarker for patients with NSCLC. Our aim in this study was to detect the plasma levels of HOTAIR and further evaluate its diagnostic value for NSCLC. The levels of HOTAIR were measured in 105 patients with NSCLC and 80 healthy controls by quantitative real-time polymerase chain reaction. The results indicated that plasma HOTAIR levels were higher in NSCLC than in healthy controls. Besides, plasma HOTAIR levels were associated with histology subtype (P = .039) and tumor-node-metastasis stage (P = .022). The ROC curves showed that plasma HOTAIR has high diagnostic accuracy for NSCLC, and the area under curve (AUC) for NSCLC versus healthy was 0.791 (95% CI: 0.727-0.855) which was higher than carcinoembryonic antigen (CEA) (AUC = 0.737, 95% CI: 0.666-0.808). Moreover, the combination of HOTAIR and CEA could provide a more accurate diagnosis than HOTAIR or CEA alone (AUC = 0.841, 95% CI: 0.783-0.898). Plasma HOTAIR levels were significantly lower in postoperative samples than in preoperative samples. Plasma HOTAIR could serve as a promising biomarker for diagnosing and monitoring NSCLC.
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