Background Growing evidence suggests that suppressor of tumorigenicity 7 antisense RNA 1 (ST7-AS1) is an oncogenic long noncoding RNA (lncRNA). However, little is known on its clinical significance, biological functions, or molecular mechanisms in lung adenocarcinoma (LUAD). Methods The expression of ST7-AS1 and miR-181b-5p were examined by qRT-PCR. The correlations between ST7-AS1 level and different clinicopathological features were analysed. In vitro, LUAD cells were examined for cell viability, migration and invasion by MTT, wound healing and Transwell assay, respectively. Epithelial-mesenchymal transition (EMT) biomarkers were detected by Western blot. The regulations between ST7-AS1, miR-181b-5p, and KPNA4 were examined by luciferase assay, RNA immunoprecipitation, RNA pulldown. Both gain- and loss-of-function strategies were used to assess the importance of different signalling molecules in malignant phenotypes of LUAD cells. The in vivo effect was analysed using the xenograft and the experimental metastasis mouse models. Results ST7-AS1 was upregulated in LUAD tissues or cell lines, correlated with tumours of positive lymph node metastasis or higher TNM stages, and associated with shorter overall survival of LUAD patients. ST7-AS1 essentially maintained the viability, migration, invasion, and EMT of LUAD cells. The oncogenic activities of ST7-AS1 were accomplished by sponging miR-181b-5p and releasing the suppression of the latter on KPNA4. In LUAD tissues, ST7-AS1 level positively correlated with that of KPNA4 and negatively with miR-181b-5p level. In vivo, targeting ST7-AS1 significantly inhibited xenograft growth and metastasis. Conclusions ST7-AS1, by regulating miR-181b-5p/KPNA4 axis, promotes the malignancy of LUAD cells. Targeting ST7-AS1 and KPNA4 or up-regulating miR-181b-5p, therefore, may benefit the treatment of LUAD.
Abstract. Esophageal squamous cell carcinoma (ESCC) is a common cancer in China and certain other parts of the world with a dismal prognosis for affected patients. AXL is a member of the TYRO3-AXL-MER family of receptor tyrosine kinases, and has been revealed to be an important mediator of epithelial-mesenchymal transition (EMT) in several types of cancer. However, to the best of our knowledge, its function in EMT in ESCC cells has not yet been examined. The present study employed two independent ESCC mRNA profile datasets and revealed that AXL is associated with several EMT markers. Gene Set Enrichment Analysis indicated that EMT occurs more in ESCC with high AXL expression. Analysis on another dataset demonstrated further that increased expression of AXL in ESCC is associated with increased migratory ability. Collectively, the results of the present study provide evidence that AXL is a marker for EMT in ESCC.
Background Long intergenic non-coding RNA 00963 (LINC00963) is an oncogenic lncRNA in human cancers. However, little is known on how it impacts the pathogenesis of lung adenocarcinoma (LUAD). Methods Biological effects on proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) were examined by CCK-8, colony formation, EdU incorporation, transwell, and immunofluorescence assays, respectively. Macrophage polarization was evaluated by flow cytometry. Ubiquitination of Zeb1 was examined by co-immunoprecipitation. The location of LINC00963 in LUAD tissues and cell lines was tested by FISH assay. The LINC00963/HNRNPA2B1/Siah1 mRNA complex interaction was verified using RNA pull-down and immunoprecipitation assays. The exact roles of LINC00963 were further validated in metastasis and xenograft models. Results Higher LINC00963 expression in LUAD patients positively correlated with shorter overall survival, higher stages, and metastasis. LINC00963 mainly localized in the cytoplasm and aggravated malignant phenotypes of LUAD cells in vitro and metastasis in vivo. Mechanistically, LINC00963 directly interacted HNRNPA2B1 protein to trigger the degradation of Siah1 mRNA, which inhibited the ubiquitination and degradation of Zeb1. Moreover, exosomal LINC00963 derived from LUAD cells induced M2 macrophage polarization and promoted LUAD growth and metastasis. Conclusion By stabilizing Zeb1 in cancer cells and delivering exosomes to induce M2 macrophage polarization, LINC00963 promoted the malignancy and metastasis of LUAD. Targeting LINC00963 may become a valuable therapeutic target for LUAD.
The purpose of our study was to evaluate the clinical efficacy of fast-track surgery (FTS) in the treatment of esophageal cancer patients combined with metabolic syndrome. Ninety-four esophageal cancer patients with metabolic syndrome were selected in Affiliated Hospital of Jining Medical University from March, 2016 to February, 2017. Patients were randomly divided into control group and observation group with 47 cases in each group. Patients in observation group were treated with FTS, while patients in control group were treated with traditional method. Intraoperative blood loss, the number of dissected lymph nodes, operation time, postoperative hospital stay, the cost of hospitalization, postoperative readmission rate, and incidence of postoperative complications were compared between the groups. Levels of serum inflammatory cytokines (TNF-α and hs-CRP), fat cell factor chemerin and leptin (LP) were detected by enzyme-linked immunosorbent assay (ELISA) at 1 month after surgery. Levels of serum total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) at 1 month after surgery were compared between groups. Levels of hemoglobin (Hb), albumin (Alb), prealbumin (PAB) and transferrin (TRF) at 1 month after surgery were also compared between the two groups. Treatment of cancer quality-of-life questionnaire-esophageal cancer (OES-18) module was used to evaluate the symptoms of patients at one month after surgery. It turned out that no significant differences in intraoperative blood loss, operation time and the number of dissected lymph nodes were found between groups (p>0.05). Postoperative hospital stay, the cost of hospitalization, postoperative readmission rate and the incidence of postoperative complications were significantly lower in observation group than in control group (p<0.05). Levels of TNF-α, hs-CRP, chemerin and LP in observation group were significantly lower than those in control group at one month after surgery (p<0.05). Levels of TC, TG and LDL-C were significantly lower and HDL-C level was significantly higher in observation group than in control group at one month after surgery (p<0.05). Levels of Hb and Alb were significantly lower and levels of PAB and TRF were significantly higher in observation group than in control group at one month after surgery (p<0.05). OES-18 score of observation group was significantly better than that of control group at one month after surgery (p<0.05). As a conclusion, FTS can promote postoperative rehabilitation, shorten hospital stay, reduce economic burden and reduce the rehospitalization rate of esophageal cancer patients. At the same time, FTS can also improve the lipid metabolism, nutritional status and regulate the differentiation of adipocytes, alleviate the low inflammatory response state, which in turn promotes metabolic syndrome.
The aim of this study was to determine the efficacy and toxicity of pemetrexed plus dendritic cells (DCs) in patients suffering from stage IIIB or IV lung adenocarcinoma, who had undergone maintenance treatment with gefitinib or erlotinib. Patients who had failed gefitinib or erlotinib maintenance treatment had ECOG performance statuses ranging from 0 to 2.27 patients received pemetrexed plus DCs as second-line treatment. Dosage: 500 mg/m(2) pemetrexed was administered on day 1 of a 21-day cycle. DCs were given for one cycle of 21 days. Three patients (11.1 %) experienced a partial response and 14 patients (51.9 %) showed stable disease. Ten patients (37.0 %) had progressive disease. The median time to progression-free survival (PFS) was 4.8 months [95 % confidence interval (CI) 4.4-5.2], and the median overall survival was 10.7 months (95 % CI 10.3-11.2). In the subgroup analysis, PFS had a significant difference between the low ratio of CD4/CD8 and normal ratio of CD4/CD8, with 4.5 months (95 % CI 4.2-4.9) and 5.0 months (95 % CI 4.5-5.7), (Log Rank = 0.039), respectively. No one patient experienced grade 4 toxicity. A regimen of pemetrexed combined with DCs is marginally effective and well tolerated in patients with stage IIIB or IV lung adenocarcinoma who had received gefitinib or erlotinib first-line treatment.
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