T-cell immunoglobulin- and mucin domain-3-containing molecule 3 (TIM-3) is a membrane protein expressed in various kinds of immune cells and plays a pivotal role in immune regulation. Recently, TIM-3 was reported to be expressed aberrantly in melanoma cells, contributing to the low adhesion ability of tumor cells and promoting the survival of melanoma cells. We investigated TIM-3 expression in non-small cell lung cancers (NSCLCs), and further analyzed whether the aberrant expression of TIM-3 is related to the prognosis for patients with lung cancer. Tumor tissue samples from 30 patients with NSCLC were involved. Results of immunohistochemical analysis showed that TIM-3 stained positive on tumor cells in 86.7% (26/30) patients with primary NSCLC. The TIM-3 expression in NSCLC tumor cells was correlated with histologic type and pathologic T classification of the disease (P < .05). More importantly, patients with TIM-3-positive tumor cells had a significantly shorter survival time than those with TIM-3-negative tumors. Multivariate analysis demonstrated the significant role of TIM-3 expression in tumor cells as an independent prognostic factor for patients with NSCLC (relative risk, 4.481; 95% confidence interval, 1.790-11.22; P = .0005). Our results suggest that the ectopic expression of TIM-3 in tumor cells may be a potential, independent prognostic factor for patients with NSCLC.

We investigated the number of intratumoral tumor-infiltrating lymphocytes (TILs), including CD4(+), CD8(+), and CD25(+) T cells, in nonsmall cell lung cancers (NSCLC) and their correlation with patient survival time. Tumor specimens from 30 NSCLC patients were consecutively obtained during surgery. Patient survival status was monitored. Based on survival time, patients were divided into 2 groups: 5-year survival group and 5-year nonsurvival group. CD4(+), CD8(+), and CD25(+) T cells that infiltrated tumors were detected and counted by immunohistochemistry. Patients with a lower number of TILs and CD8(+) T cells showed significantly shorter survival time compared with those with a higher number (P < 0.05). However, the number of CD4(+) and CD25(+) T cells in tumors was not correlated with survival time in patients with NSCLC (P > 0.05). These data demonstrate that high numbers of CD8(+) T cells among TILs is a strong indicator for a favorable clinical outcome.

Syncytin-1 is a protein coded by a human endogenous retrovirus (HERV) gene of the HERV-W family (HERVWE1). Syncytin- 1 mediates formation of syncytiotrophoblasts through fusion of cytotrophoblasts, a hallmark of terminal differentiation of placental trophoblast linage. Syncytin-1 also possesses nonfusogenic functions and regulates cell cycle progression. While decreased syncytin-1 expression and syncytium deficiency are considered important pathological changes in preeclampsia, the molecular mechanism(s) underlying syncytin-1 downregulation remains unclear. In this study, we confirmed that expression levels of syncytin-1 mRNA and protein were significantly lower in preeclamptic placentas compared to normal controls. Human chorionic somatomammotropin expression, a marker for syncytium function, was also decreased in preeclamptic placentas. The mRNA levels of ASCT2, the syncytin-1 receptor involved in cell fusion process, and GCMa, a transcriptional factor known to regulate syncytin-1 expression, were not significantly altered. Methylation in the 5'LTR of syncytin-1 promoter was quantified by COBRA, methylation-specific PCR, and DNA sequencing. Results from all three assays indicated significantly hypermethylated syncytin-1 promoter in preeclamptic placentas compared to normal controls. Methylation levels were inversely correlated with syncytin-1 mRNA levels, suggesting that hypermethylation may lead to syncytin-1 downregulation. Further experiments indicated that DNMT1 and DNMT3B3 mRNA and protein levels were increased in preeclamptic placentas, suggesting that higher DNA methyltransferase activity may contribute to the hypermethylation of syncytin-1 in preeclamptic placentas. These results indicated that aberrant hypermethylation is involved in downregulation of syncytin-1, and epigenetic alterations may play a significant role in the development of preeclampsia.

Our finding can increase the rational allocation of nurse-patient ratio and provide personalised nursing for severe patients to reduce complications and promote the rehabilitation of the disease. Our findings can also serve as a reference for other countries to develop the nurse practitioner role.

Syncytin 1 is considered as an oncogene in various malignant tumors, but its effect on non‐small cell lung cancer (NSCLC) has not been reported. We investigated the specific role of Syncytin 1 on NSCLC through the transfection of Syncytin 1 knockdown or overexpression plamids in A549 cells. Our results proved that knockdown of Syncytin 1 inhibited the proliferation, and blocked the cell cycle on G1 phase by inhibiting the expression of Nusap1, Cyclin D1, CDK6, and CDK4. Cell cycle arrest also leaded to increased apoptosis in Syncytin 1 knockdown cells. Suppression of Syncytin 1 inhibited the migration and invasion, as well as the expressions of epithelial‐mesenchymal transition (EMT) makers, N‐cadherin, β‐catenin, and Vimentin, indicating that Syncytin 1 knockdown inhibited the metastasis via reversing the EMT process in A549 cells. The phosphorylation levels of Akt, mTOR, and Erk1/2 were all decreased in Syncytin 1 knockdown cells, suggesting the signaling pathways by which Syncytin 1 operated as an oncogene in NSCLC. Moreover, the underexpression of transcription factor SP1 downregulated the Syncytin 1 expression in A549 cells. The rescue experiment of Syncytin 1 in SP1 knockdown cells further proved that Syncytin 1 could block the inhibition of cell growth induced by SP1 knockdown. In conclusion, knockdown of SP1/Syncytin1 axis inhibited the progression of NSCLC by the reversion of tumor epithelial‐mesenchymal transition process and suppression of Akt and Erk signaling pathways, suggesting that they are potential targets for targeted therapy of NSCLC.