The number of esophageal cancer patients is increasing worldwide and lots of patients suffer from malnutrition and hypoalbuminemic. Serum albumin is a widely acceptable method of assessing nutritional and inflammation status in cancer patients. But whether serum albumin has prognostic value with regard to short-term and long-term outcomes in patients who undergo esophagectomy for cancer is still unclear. We therefore investigated the prognostic role of serum albumin in patients with esophageal cancer. We retrospectively reviewed 208 patients who underwent esophagectomy from September 1, 2003 to December 31, 2008. Clinico-pathological characteristics and postoperative outcomes were compared between different pretherapeutic serum albumin classes: low (hypoalbuminemic), <35 g/l; middle, 35-40 g/l and high, >40 g/l. Older, female, and higher T-stages were more likely to be associated with hypoalbuminemic. Meanwhile, hypoalbuminemic patients had a higher rate of postoperative mortality and complications including sepsis, respiratory insufficiency, arrhythmia, and cardiac insufficiency. But for preoperative comorbidities, no significant difference was found between different pretherapeutic serum albumin classes. The overall 5-year survival rate was 28.6%, 43.9%, and 50.8% for patients with low, middle, and high pretherapeutic serum albumin levels, respectively. Hypoalbuminemic was associated with poor survival (P = 0.016). In a multivariate analysis, the pretherapeutic albumin level was proved to be an independent predictor of survival (hazard ratio = 0.731; 95% confidence interval: 0.544-0.982, P = 0.037). Pretherapeutic serum albumin level is a significant prognostic factor for short-term and long-term outcomes in patients who undergo esophagectomy for cancer, which therefore should be taken into consideration along with other well-defined prognostic factors for better preoperative assessment and prognostic evaluation.

Infection and inflammation serve an important role in tumor development. Toll-like receptor 4 (TLR4) is a pivotal component of the innate and adaptive immune response during infection and inflammation. Programmed-death ligand 1 (PD-L1) is hypothesized as an important factor for non-small cell lung cancer (NSCLC) immune escape. In the present study, the relationship between TLR4 and PD-L1, in addition to the associated molecular mechanism, were investigated. TLR4 and PD-L1 expression in lung cancer tissues were detected using immunohistochemistry, whilst overall patient survival was measured using the Kaplan-Meier method. The A549 cell line stimulated using lipopolysaccharide (LPS) was applied as the in vitro inflammatory NSCLC model. Associated factors were investigated using reverse transcription-quantitative PCR and western blotting. Lung cancer tissues exhibited increased PD-L1 and TLR4 levels compared with those of adjacent para-cancerous tissues, where there was a positive correlation between TLR4 and PD-L1 expression. In addition, increased expression of these two proteins was found to be linked with poorer prognoses. Following the stimulation of A549 cells with LPS, TLR4 and PD-L1 expression levels were revealed to be upregulated in a dose-dependent manner, where the ERK and PI3K/AKT signaling pathways were found to be activated. Interestingly, in the presence of inhibitors of these two pathways aforementioned, upregulation of PD-L1 expression was only inhibited by the MEK inhibitor PD98059, which can inhibit ERK activity. These data suggested that the ERK signaling pathway is necessary for the TLR4/PD-L1 axis. In conclusion, data from the present study suggest that TLR4 and PD-L1 expression can serve as important prognostic factors for NSCLC, where TLR4 activation may induce PD-L1 expression through the ERK signaling pathway.

Esophageal squamous cell carcinoma (ESCC) is recognized as one of the malignant tumors with poor prognosis. UAP1L1 (UDP‐N‐acetylglucosamine‐1‐like‐1) affects numerous biological processes, which is a key regulator of the development of malignant tumors. The biological function and molecular mechanism of UAP1L1 in ESCC were explored in this study. The relationship between UAP1L1 and ESCC was analyzed by immunohistochemical staining, revealing the high expression of UAP1L1 in ESCC. Importantly, the increased expression of UAP1L1 indicated the deterioration of patients’ condition, which has clinical significance. Furthermore, the loss‐of‐function assays demonstrated that knockdown of UAP1L1 inhibited the progression of ESCC on suppressing proliferation, hindering migration, and enhancing apoptosis in vitro. Moreover, the apoptosis of ESCC cells was induced by knockdown of UAP1L1 via regulating a variety of apoptosis‐related proteins, such as upregulation of Bax, CD40, CD40L, Fas, FasL, IGFBP‐6, p21, p27, p53, and SMAC. Additionally, further investigation indicated that UAP1L1 by affecting the PI3K/Akt, CCND1, and MAPK promotes the progression of ESCC. In vivo xenograft model further confirmed that knockdown of UAP1L1 inhibited the development of ESCC. In conclusion, UAP1L1 was involved in the development and progression of ESCC, which may provide a powerful target for future molecular therapies.

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