Abstract. The programmed death-1 (PD-1)/programmed death-ligands (PD-Ls) signal pathway has been implicated as a potential immune escape mechanism in several human cancers. However, the studies of PD-1/PD-Ls pathway in esophageal squamous cell carcinoma (ECSS) are not yet sufficient. The current study investigated the expression of PD-L1, PD-L2 and PD-1 in ESCC tissues. The correlations between the expression of these proteins and clinical histopathological parameters were analyzed. Then the stable transfected Ec109 cell lines overexpressing PD-L1/PD-L2 were established by plasmid transfection successfully. Ec109 and CD8 + T cells were co-cultured to analyze the effects of PD-1/PD-Ls signal pathway on the function of CD8 + T cells including proliferation, apoptosis and interferon-γ production. We found that PD-L1-positive patients had significantly poorer prognosis than the negative patients, while their prognosis was not related to PD-L2 expression. The count of PD-1 + TILs (tumor-infiltrating lymphocytes) was negatively correlated with both PD-L1 and PD-L2 expression. In functional studies, we found that PD-1/PD-Ls signal pathway was able to downregulate the function of CD8 + T lymphocyte and its function could be restored by blocking the signal pathway. This indicates that PD-1/PD-Ls may prevent effective antitumor immunity, which provides important evidence to delineate the cellular immune deficiency mechanism in ESCC. Therefore, PD-1/PD-Ls are predicted to become novel targets for ESCC immunotherapy.
Esophageal squamous cell carcinoma (ESCC) is a common histologic subtype in China. It has been suggested that abnormal expression of microRNAs (miRNAs) is associated with carcinogenesis. We investigated miR-126 expression and its potential targets in ESCC. The expression of miR-126 was detected in cancerous and paired paracancer tissues from 102 patients with ESCC. Target analysis of miR-126 was predicted using online tools. The effect of miR-126 expression on target proteins was assessed using miR-126 mimics or miR-126 inhibitors in ESCC cell lines. In addition, the impact of miR-126 on cell proliferation, apoptosis, migration and invasion was detected in ESCC cell lines. The expression of miR-126 was significantly lower in ESCC tissues, which was associated with tumor differentiation, lymph node metastasis, tumor in-depth and TNM stage. Insulin receptor substrate-1 (IRS-1) and Golgi phosphoprotein 3 (GOLPH3) were overexpressed in ESCC. Overexpression of IRS-1 was associated with cell differentiation, whereas GOLPH3 was related to lymph node metastasis, tumor invasion in-depth and TNM stage in ESCC patients. miR-126 mimics downregulated the expression of IRS-1 and GOLPH3 protein and suppressed the proliferation, migration and invasion of ESCC cells, whereas miR-126 inhibitors led to the opposite results. miR-126 suppressed the proliferation, migration and invasion of ESCC cells, and acted as a tumor suppressor in the carcinogenesis of ESCC. IRS-1 and GOLPH3 are downstream targets of miR-126 at the post-transcriptional level in ESCC.
Double-lumen endotracheal tube (DLET) anaesthesia is the commonly used method in minimally invasive oesophagectomy (MIE). However, DLET intubation does have its disadvantages. Firstly, the placement of the DLET needs a skilled anaesthetist with familiarity of the technique and subsequent ability to perform a fibre-optic bronchoscopy for confirmation. Secondly, DLET intubation and one-lung ventilation are associated with numerous complications, including hoarseness, tracheobronchial injury and vocal injury. In this report, a retrospective analysis was performed on 42 consecutive patients who underwent MIE using single-lumen endotracheal tube (SLET) anaesthesia with CO2 artificial pneumothorax compared with 81 patients who underwent the same procedure with DLET intubation. Our findings showed that SLET intubation with artificial pneumothorax by CO2 insufflation is a feasible and safe method for MIE procedures.
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