Background: A growing body of evidence indicates that long non-coding RNAs (lncRNAs) can act as competitive endogenous RNAs (ceRNAs) to bind to microRNAs (miRNAs), thereby affecting and regulating the expression of target genes. The lncRNA-miRNA-mRNA ceRNA network has been theorized to play an indispensable role in many types of tumors. However, the role of the lncRNA-related ceRNA regulatory network in lung adenocarcinoma (LUAD) remains unclear. Methods: We downloaded the RNAseq and miRNAseq data of LUAD from The Cancer Genome Atlas (TCGA) data portal and identified differentially expressed lncRNAs (DElncRNAs), differentially expressed miRNAs (DEmiRNAs), and differentially expressed mRNAs (DEmRNAs) between LUAD and corresponding paracancerous tissues by using the edgeR package of R software. We constructed the lncRNA-miRNA-mRNA ceRNA network by using Cytoscape (version 3.7.2) on the basis of the interaction generated from the miRcode, miRTarBase, miRDB, and TargetScan databases. Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed with DAVID 6.8 bioinformatics resources and plotted by using the ggplot2 package in R. The effect of genes on LUAD prognosis was assessed by applying the survival package in R in accordance with the Kaplan-Meier curve. Results: In total, 1645 DElncRNAs, 117 DEmiRNAs, and 2729 DEmRNAs were identified in LUAD. The LUAD-specific ceRNA network was composed of 157 nodes and 378 edges (329 DElncRNA-DEmiRNA interactions and 49 DEmiRNA-DEmRNA interactions). GO and KEGG pathway annotations suggested that the LUAD-specific ceRNA network was related to tumor-related molecular functions and pathways.

Growing evidence indicates that systemic inflammation response and malnutrition status are correlated with survival in certain types of solid tumors. The aim of this study is to evaluate the association between the systemic immune-inflammation index (SII) and prognostic nutritional index (PNI) and overall survival (OS) in patients with esophageal squamous cell carcinoma (ESCC) after esophagectomy. A consecutive series of 655 patients with resected ESCC who underwent esophagectomy were enrolled in the retrospective study. The preoperative SII was defined as platelet × neutrophil/lymphocyte counts. The PNI was calculated as albumin concentration (g/L) + 5 × total lymphocyte count (10 /L). The optimal cut-off values of SII, neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and PNI were determined by receiver operating characteristic analysis. Survival analysis was performed using the Kaplan-Meier method with a log-rank test, followed by a multivariate Cox proportional hazards model. A high SII was significantly related to tumor size, histological type, invasion depth, and TNM stage (p < 0.05). A low PNI was significantly associated with age, tumor size, invasion depth, lymph node metastasis, and TNM stage (p < 0.05). Univariate analysis revealed that age, smoking history, tumor size, invasion depth, lymph node metastasis, SII, NLR, PLR, and PNI were predictors of OS (p < 0.05). Multivariate analysis identified age (p = 0.041), tumor size (p = 0.016), invasion depth (p < 0.001), lymph node metastasis (p < 0.001), SII (p = 0.033), and PNI (p = 0.022) as independent prognostic factors correlated with OS. There was a significant inverse relationship between the SII and PNI (r = 0.309; p < 0.001). The predictive value increased when the SII and PNI were considered in combination. Our results demonstrate that the preoperative high SII and low PNI are powerful indicators of aggressive biology and poor prognosis for patients with ESCC. The combination of SII and PNI can enhance the accuracy of prognosis.

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Effective analysis of E-cadherin and S100A4 expression may allow for the identification of patients who are at a high risk of recurrence and poor prognosis in SqCC.

Obesity is closely related to a poor prognosis in patients with advanced colorectal cancer (CRC), but the mechanisms remain unclear. Ferroptosis is a form of nonapoptotic cell death characterized by lipid reactive oxygen species (ROS) accumulation and iron dependency and is associated with the chemoresistance of tumors. Here, it is shown that adipose‐derived exosomes reduce ferroptosis susceptibility in CRC, thus promoting chemoresistance to oxaliplatin. It is found that microsomal triglyceride transfer protein (MTTP) expression is increased in the plasma exosomes of CRC patients with a high body fat ratio, serving as an inhibitor of ferroptosis and reducing sensitivity to chemotherapy. Mechanistically, the MTTP/proline‐rich acidic protein 1 (PRAP1) complex inhibited zinc finger E‐box binding homeobox 1 expression and upregulated glutathione peroxidase 4 and xCT, leading to a decreased polyunsaturated fatty acids ratio and lipid ROS levels. Moreover, experiments are carried out in organoids, and a tumor implantation model is established in obese mice, demonstrating that the inhibition of MTTP increases the sensitivity to chemotherapy. The results reveal a novel intracellular signaling pathway mediated by adipose‐derived exosomes and suggest that treatments targeting secreted MTTP might reverse oxaliplatin resistance in CRC.

Primary adenosquamous carcinoma (ASC) of the esophagus is a rare kind of malignancy characterized by mixed glandular and squamous differentiation as well as a propensity for aggressive clinical behavior. Data on the evaluation of the clinicopathological features and the prognosis of patients suffering from this malignancy are few because of the rarity of this disease. We conducted a retrospective review of 24 patients with primary esophageal ASC among 6546 esophageal cancer patients who underwent transthoracic esophagectomy in our hospital. The clinicopathological presentation, diagnosis, treatment, and prognostic factors of the patients were respectively investigated. The Kaplan-Meier method and the log rank test were used to calculate and compare overall survival (OS). The Cox proportional hazards model was employed to identify independent prognostic factors. There were 18 males and 6 females with a median age of 60 years (range: 40-78 years). The clinical symptoms, macroscopic type, as well as the radiological and endoscopic features of esophageal ASC were similar to those of esophageal squamous cell carcinoma. Sixteen (88.9%) of the 18 cases who underwent preoperative esophagoscopic biopsy were misdiagnosed as adenocarcinoma or squamous cell carcinoma. The overall median follow-up period was 36 months, and the median survival time was 32 months. The 1, 3, 5-year OS rates were 75.0%, 48.5%, and 19.4%, respectively. Univariate analysis showed that gender (P=0.047), lymph node metastasis (P=0.007), and TNM stage (P=0.037) were important factors associated with OS of the 22 patients who underwent radical resection. Multivariate analysis showed that the pathological N stage was the only independent prognostic factor (P=0.031, hazard ratio [HR], 5.369, 95% confidence interval [CI], 1.167-24.700). These results suggest that esophageal ASC is an uncommon disease prone to be misdiagnosed by endoscopic biopsy. Surgical resection is the primary treatment, but the prognosis of ASC is usually poorer than conventional squamous cell carcinoma. Lymph node metastasis is an independent prognostic factor after radical resection.

As a mitotic spindle checkpoint gene, baculoviral IAP repeat containing 5 (BIRC5) serves pivotal roles in the development of various types of malignant tumors. In the present study, the expression of BIRC5 in patients with different stages of esophageal squamous cell cancer (ESCC) was investigated. The effect of BIRC5 on the migratory and invasive abilities of different ESCC cell lines was analyzed. Additionally, the effect of BIRC5 on the angiogenesis-associated factor vascular endothelial growth factor, brain-specific angiogenesis inhibitor 1 and methyl-CpG binding domain protein 2 was examined. In addition, the interaction between BIRC5 and the phosphatidylinositol 3-kinase (PI3K)/Akt pathway was analyzed. It was determined that BIRC5 is able to inhibit the migration and invasion of tumor cells, and regulate the expression of angiogenesis-associated factors. In addition, the PI3K/Akt signaling pathway is able to regulate the expression of BIRC5, which affects the development of ESCC.

Background: CirRNA Circ_0058063 has been proven as an oncogene in bladder cancer, while its involvement in esophageal squamous-cell carcinomas (ESCC) is unknown. This study aimed to investigate the role of Circ_0058063 in ESCC. Methods: Paired ESCC and non-tumor tissues were collected from ESCC patients and gene expression was analyzed by quantitative reverse transcription polymerase chain reaction (RT-qPCR). Gene interactions were analyzed by overexpression experiment. Glucose uptake was analyzed by glucose uptake assay. Cell proliferation was analyzed by cell proliferation assay. Results: We found that Circ_0058063 was upregulated in ESCC and positively correlated with GLUT1 mRNA. It is known that GLUT1 plays critical roles in glucose transportation and glucose supports the Warburg Effect as the major metabolic precursor. In ESCC cells, Circ_0058063 and GLUT1 overexpression both promoted glucose uptake. In ECSS cells, Circ_0058063 overexpression resulted in the upregulated, while Circ_0058063 knockdown resulted in downregulated GLUT1. In cell proliferation assay, Circ_0058063 and GLUT1 overexpression resulted in the increased, while Circ_0058063 knockdown resulted in the decreased rate of ESCC cell proliferation. Moreover, GLUT1 overexpression reduced the effects of Circ_0058063 knockdown. Conclusions: Circ_0058063 upregulates GLUT1 expression and promotes glucose-uptake in ESCC to promote cell proliferation.