Risk factors of atrial fibrillation occurring after radical surgery of esophageal carcinoma.

BACKGROUND: Atrial fibrillation (AF) is a common complication after radical surgery of esophageal cancer. The aim of this study was to explore AF risk factors after radical surgery of esophageal carcinoma. METHOD: The data of 335 patients with esophageal cancer who were admitted in our hospital from January 2014 to August 2016 for the first time were retrospectively analyzed. We retrieved the papers in some data banks using the search terms including English and Chinese search terms, and obtained 13 factors which were mentioned in more than 6 papers. The 13 factors including age, gender, history of smoking, history of hypertension, history of peripheral vascular disease, history of cardiac stents or angina pectoris, preoperative pulmonary infection, preoperative brain natriuretic peptide (BNP) level, preoperative left ventricular diastolic dysfunction, operative method, lesion location, intraoperative blood transfusion, adhesion between lymph nodes and pericardium, underwent univariate and multivariate analyses. RESULTS: Of the 335 patients with esophageal cancer, 48 had AF within one week after operation. Univariate analysis indicated that the age (OR: 4.89; CI: 2.53-9.47, P: 0.000), gender (OR: 2.26; CI: 1.17-4.37, P: 0.013), history of peripheral vascular disease (OR: 2.29; CI: 1.06-4.92, P: 0.030), history of cardiac stents or angina pectoris (OR: 27.30; CI: 12.44-59.91, P: 0.000), preoperative BNP level (OR: 27.13; CI: 10.97-67.06, P: 0.000), preoperative left ventricular diastolic dysfunction (OR: 2.22; CI: 1.19-4.14, P: 0.012), operative method (OR: 2.09; CI: 1.002-4.380, P: 0.046), intraoperative blood transfusion (OR: 20.24; CI: 8.39-48.82, P: 0.000), and adhesion between lymph nodes and pericardium were risk factors (OR: 2.05; CI: 1.08-3.87, P: 0.024). Furthermore, multivariate analysis displayed that advanced age (OR: 5.044; CI: 1.748-14.554, P: 0.003), male (OR: 6.161; CI: 2.143-17.715, P: 0.001), history of cardiac stents or angina pectoris (OR: 48.813; CI: 13.674-174.246, P: 0.000), preoperative BNP > 100 (OR: 41.515; CI: 9.380-183.732, P: 0.000), open surgery (OR: 3.357; CI: 1.026-10.983, P: 0.045), intraoperative blood transfusion (OR: 58.404; CI: 10.777-316.509, P: 0.000), and adhesion between lymph nodes and pericardium (OR: 3.954; CI: 1.364-11.459, P: 0.011) were risk factors which could increase the incidence of postoperative AF. CONCLUSION: We should pay attention to the above risk factors in order to reduce the incidence of postoperative AF.

Expression and Effects of Long Non-Coding RNA, LINC01124, in Non-Small Cell Lung Cancer.

OBJECTIVE: To investigate the expression and evaluate the clinical significance of long non-coding RNA, LINC01124, in non-small cell lung cancer (NSCLC) and to study its influence in this tumor. METHODS: Hundred specimens of NSCLC tissues and normal lung tissues after surgery were collected. The qRT-PCR for LINC01124 expression was performed on cancerous and normal lung tissues. The correlations between the expression of LINC01124 and pathological characteristics were analyzed. PcDNA-LINC01124 was transfected to upregulate LINC01124 expression in NSCLC cells, and the transfection efficiency was evaluated by the qRT-PCR. CCK8 assay, wound-healing assay, and the Transwell assay were performed to evaluate the effect of ectopic LINC01124 expression on proliferation, migration, and invasive of NSCLC cells. RESULTS: The expression level of LINC01124 was downregulated in tumor tissues when compared with the paired normal lung tissues (P<0.05). The expression of LINC01124 was associated with patients' age and distant metastasis (P<0.05). Enforced expression of LINC01124 significantly inhibited the proliferation, migration, and invasive ability of NSCLC cells. CONCLUSION: The expression of LINC01124 was decreased in patients with NSCLC of older age and with those having distant metastasis. LINC01124 may inhibit cell proliferation, migration, and invasive ability.

The long non-coding RNA MIAT regulates zinc finger E-box binding homeobox 1 expression by sponging miR-150 and promoteing cell invasion in non-small-cell lung cancer.

The myocardial infarction associated transcript (MIAT), a long non-coding RNA (lncRNA), was originally identified as a candidate gene for myocardial infarction, and was recently shown to participate in the progression of cancer and the process of metastasis. However, the biological role of MIAT and the underlying mechanisms that mediate its role in non-small-cell lung cancer (NSCLC) remain unclear. Here, we have shown that the expression of MIAT in NSCLC tissues was upregulated. Knockdown of MIAT substantially inhibited the invasive ability of NSCLC cells. Moreover, the knockdown of MIAT significantly downregulated the expression of the zinc finger E-box binding homeobox 1 (ZEB1), that was upregulated in NSCLC and that promoted cell invasion. Rather than by direct interactions, we found that MIAT indirectly regulated ZEB1 expression through sponging and suppressing microRNA (miR)-150, which represses ZEB1 and interacts with MIAT in a sequence-specific manner. Thus, MIAT may inhibit ZEB1 expression and promote cell invasion of NSCLC cells via the miR-150/ZEB1 pathway. Taken together, our findings suggested that MIAT plays an oncogenic role in NSCLC through the ZEB1 signaling pathway by sponging miR-150, and MIAT may therefore serve as a valuable prognostic biomarker and therapeutic target for NSCLC.

Knockdown of GluA2 induces apoptosis in non-small-cell lung cancer A549 cells through the p53 signaling pathway.

α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors are important glutamatergic receptors that mediate fast excitatory synaptic transmission in the brain. Previous studies have demonstrated that glutamate ionotropic receptor AMPA type subunit 2 (GluA2), one of the four subunits that comprise AMPA receptors, is a potential novel marker for poor prognosis in patients with human lung cancer. However, the mechanisms of GluA2-induced apoptosis, proliferation and migration in lung cancer remain unknown. The present study aimed to explore the mechanisms underlying these effects of GluA2 in human lung cancer by silencing GluA2 in A549 cells. Using the Cell Counting Kit-8 assay, western blot analysis and acridine orange/ethidium bromide staining, downregulation of GluA2 was revealed to significantly inhibit the proliferation and significantly promote the apoptosis of A549 cells. Knockdown of GluA2 was also revealed to be associated with increased caspase-3 activity, increased Bcl-2-associated X protein and Bcl-2-associated death promoter (Bad) expression, and decreased expression of B-cell lymphoma-2, p-Bad and X-linked inhibitor of apoptosis protein. In addition, GluA2 silencing upregulated cellular tumor antigen p53 (p53)/p21Cip1/Waf1/p16INK4a protein. In conclusion, these results indicate that the effects of GluA2 in lung cancer are mediated by the caspase-3 and p53/p21Cip1/Waf1/p16INK4a signaling pathways. Therefore, GluA2 may be a potential novel therapeutic target for the treatment of lung cancer.

Long non-coding RNA SNHG1 regulates zinc finger E-box binding homeobox 1 expression by interacting with TAp63 and promotes cell metastasis and invasion in Lung squamous cell carcinoma.

The long non-coding RNAs (lncRNAs) have been recently shown to participate in the progression of a variety of cancers. However, the biological role of lncRNAs and the underlying mechanisms in Lung squamous cell carcinoma (SCC) or lung adenocarcinoma (AD) remain unclear. Herein, we investigated expression of 5 lncRNAS (SNHG1, NCBP2-AS2, LINC01206, SOX2-OT and LINC01419) in SCC and AD tissues. SNHG1 was one of over-expressed lncRNAs in SCC tissues. Knockdown of SNHG1 significantly inhibited the proliferation, metastasis, invasive ability and induced apoptosis of SCC cells. Moreover, SNHG1 affected the expression of zinc finger E-box binding homeobox 1(ZEB1), which has also been observed to be up-regulated in SCC and to promote cell metastasis and invasion. Rather than direct interaction, SNHG1 regulated ZEB1expression by suppressing the activity of p63 TA isoform (TAp63), which is a repressor of ZEB1 and physically associates with SNHG1. Furthermore, SNHG1 promoted ZEB1 expression and promoted cell proliferation, metastasis, invasive but inhibited apoptosis of SCC cells via the TAp63/ZEB1 pathway. Taken together, our findings suggested that SNHG1 might play an oncogenic role in SCC through ZEB1 signaling pathway by inhibiting TAp63 and might serve as a valuable prognostic biomarker and therapeutic target for SCC patients.

Alpinetin inhibits lung cancer progression and elevates sensitization drug-resistant lung cancer cells to cis-diammined dichloridoplatium.

OBJECTIVE: Alpinetin is a novel flavonoid that has demonstrated potent antitumor activity in previous studies. However, the efficacy and mechanism of alpinetin in treating lung cancer have not been determined. METHODS: We evaluated the impact of different doses and durations of alpinetin treatment on the cell proliferation, the apoptosis of lung cancer cells, as well as the drug-resistant lung cancer cells. RESULTS: This study showed that the alpinetin inhibited the cell proliferation, enhanced the apoptosis, and inhibited the PI3K/Akt signaling in lung cancer cells. Moreover, alpinetin significantly increased the sensitivity of drug-resistant lung cancer cells to the chemotherapeutic effect of cis-diammined dichloridoplatium. Taken together, this study demonstrated that alpinetin significantly suppressed the development of human lung cancer possibly by influencing mitochondria and the PI3K/Akt signaling pathway and sensitized drug-resistant lung cancer cells. CONCLUSION: Alpinetin may be used as a potential compound for combinatorial therapy or as a complement to other chemotherapeutic agents when multiple lines of treatments have failed to reduce lung cancer.

Expression and clinicopathologic significance of proteolysis-inducing factor in non-small-cell lung cancer: an immunohistochemical analysis.

BACKGROUND: Proteolysis-inducing factor (PIF) is a 24-kD glycoprotein that has been identified in mice and in humans with cancer cachexia. The PIF is a putative mediator of cancer-associated weight loss, which induces atrophy of skeletal muscle. MATERIALS AND METHODS: In this study, we detected the expression of the PIF in 71 patients with non-small-cell lung cancer (NSCLC) and 10 patients with healthy lung tissues as a control group using the immunohistochemical staining method. In addition, weight loss of patients and serum carcinoembryonic antigen (CEA) and cytokeratin fragment antigen 21-1 (CYFRA 21-1) were measured, and an analysis of overall survival was done. RESULTS: Proteolysis-inducing factor was expressed in only 56.3% (40/71) of lung cancers and not in normal tissue. The positive rate of the PIF expression was significantly higher (P < .01) in patients with weight loss than in those without weight loss. There was no significant relationship (P > .05) between the PIF expression and the histology type, degree of differentiation, or tumor clinical stages in lung cancers. The sensitivity of the PIF was better than that of CEA (P < .05), but similar to that of CYFRA 21-1 in NSCLC. CONCLUSION: Proteolysis-inducing factor expression was negatively related to the survival of patients with NSCLC in the medium to advanced stages (II-IV). There was a significant correlation between weight loss and survival in the PIF-positive patients.