Removal of hydrogen sulfide in the gas phase by carbide slag modified bentonite.

Bentonite-based adsorbents for the removal of hydrogen sulfide (H2S) were prepared by a wet-mixing method using carbide slag as the active component. The effects of carbide slag content, calcination temperature, calcination time, and reaction temperature on the H2S adsorption capacity were investigated. The results showed that compared with the blank bentonite adsorbent, the carbide slag-modified bentonite-based adsorbent enhanced the chemisorption of H2S. The adsorption capacity of the carbide slag modified bentonite adsorbent (2.50 mg g-1) was more than 40 times higher than that of the blank bentonite-based adsorbent (0.06 mg g-1) under optimal conditions. The optimal conditions for H2S removal were 3 : 5 ratio of carbide slag-to-bentonite, calcination temperature of 450 °C for 2 h, and reaction temperature of 95 °C. H2S was mainly removed in the mesopores and macropores of the adsorbent and was finally transformed to CaS and sulfate on the adsorbent surface. The adsorption process of H2S followed the Freundlich adsorption isotherm equation and Bangham adsorption kinetic model.

Prognosis Value of microRNA-3677-3p in Lung Adenocarcinoma and Its Regulatory Effect on Tumor Progression.

PURPOSE: Lung adenocarcinomas (LUAD) was the most common subtype of lung cancer, and may result in a poor prognosis. This study was designed to explore the role of miR-3677-3p in LUAD and discuss in what way it functions in LUAD. MATERIALS AND METHODS: We used RT-qPCR method to detect the expression levels of miR-3677-3p in 105 pairs of LUAD tissues and noncancerous tissues, as also as in LUAD cells. We used χ 2 test to analyze the correlation between miR-3677-3p level and the clinical data. The prognosis significance of miR-3677-3p was inferred with Kaplan-Meier and multivariate Cox regression assays. Biological functions of LUAD cells were accessed by cell counting kit-8, transwell migration and invasion assay. The target gene of miR-3677-3p was investigated by luciferase activity assay. RESULTS: miR-3677-3p represented an ascendant expression in LUAD tissue specimens and cells. miR-3677-3p expression was associated with the TNM stage and with solitary metastasis. Over-expression of miR-3677-3p can shorten the overall survival period of LUAD patients when compared with low expression. Knockdown of miR-3677-3p suppressed the biology function of NSCLC cells including proliferation, migration, and invasion. KLF12 was a target gene of miR-3677-3p. CONCLUSION: miR-3677-3p represents as a potential prognostic biomarker for LUAD. miR-3677-3p can promote LUAD progression by targeting KLF12.

N6-methyladenosine (m6A) methyltransferase KIAA1429 accelerates the gefitinib resistance of non-small-cell lung cancer.

N6-methyladenosine (m6A) modification has been convincingly identified to be a critical regulator in human cancer. However, the contribution of m6A to NSCLC gefitinib resistance is still largely unknown. Here, we screened and identified that m6A methyltransferase KIAA1429 was highly expressed in gefitinib-resistant NSCLC cells (PC9-GR), tissues, and closely related to unfavorable survival. Functionally, KIAA1429 accelerated the gefitinib resistance of NSCLC in vitro. Depletion of KIAA1429 repressed the tumor growth of PC9-GR cells in vivo. Mechanistically, KIAA1429 enhanced the mRNA stability of HOXA1 through targeting its 3'-untranslated regions (3'-UTR). Overall, our findings indicate that KIAA1429 plays essential oncogenic roles in NSCLC gefitinib resistance, which may provide a feasible therapeutic target for NSCLC.

A study on the efficacy of recombinant human endostatin combined with apatinib mesylate in patients with middle and advanced stage non-small cell lung cancer.

PURPOSE: To explore the clinical efficacy of recombinant human endostatin combined with apatinib mesylate in patients with middle and advanced non-small cell lung cancer (NSCLC). METHODS: A total of 64 patients with middle and advanced NSCLC were randomly divided into the control group (n=32) and observation group (n=32). The patients in control group received paclitaxel monotherapy, while those in the observation group were treated with recombinant human endostatin combined with apatinib mesylate. The short-term efficacy, the lung function and levels of immunoglobulin and T lymphocyte subsets before and after treatment and the adverse drug reactions of patients were compared between the two groups. All patients were followed up for 5 years, and the survival rate in the two groups was observed. RESULTS: The short-term efficacy and lung function in observation group were better than those in control group (p<0.05). Compared with those in the control group, the levels of immunoglobulin G (IgG), IgA, IgM, cluster of differentiation 3+ (CD3+), CD4+ and CD4+/CD8+ were increased, while the CD8+ level was lowered in the observation group (p<0.05). The rate of adverse drug reactions in the observation group was lower than that in the control group (p<0.05). The 5-year survival rate was significantly higher in the observation group than that in the control group (p<0.05). CONCLUSION: Recombinant human endostatin combined with apatinib mesylate achieves a better therapeutic effect in the treatment of middle and advanced NSCLC, with improved immune resistance of patients and less side effects. Therefore, it is worthy of popularization and application in clinical practice.

Overexpression of GPR35 confers drug resistance in NSCLC cells by ß-arrestin/Akt signaling.

BACKGROUND: Non-small-cell lung cancer (NSCLC) is the major leading cause of cancer-related death around the world. The resistance to chemotherapy limits the effects of clinical treatment. The aim of this study was to identify novel mechanisms involved in NSCLC chemoresistance. MATERIALS AND METHODS: We explored the public database and commercial tissue microarray to evaluate the expression of G protein-coupled receptor 35 (GPR35). We established the chemoresistant A549 cell line to further investigate the biological function of GPR35 in vitro and in vivo. Then, we measured the altered signalings that GPR35 knocking down by Western blot assay. RESULTS: We demonstrated that GPR35 expression was significantly elevated in NSCLC tissues and correlated with poor prognosis. GPR35 was upregulated in our in vitro chemoresistance cell model. GPR35 depletion reduced the half maximal inhibitory concentration of chemodrugs and restored the sensitivity both in vitro and in vivo. Mechanically, we found that GPR35-mediated chemoresistance occurred partially via ß-arrestin-2/Akt signaling. Furthermore, inhibition of ß-arrestin-2 or Akt activation could suppress the GPR35 expression and overcome chemoresistance. CONCLUSION: Our results suggested that GPR35 might serve as a novel therapeutic target to enhance the chemotherapy efficacy in NSCLC.

Chemokine-like factor-like MARVEL transmembrane domain-containing 3 expression is associated with a favorable prognosis in esophageal squamous cell carcinoma.

Decreased expression of human chemokine-like factor-like MARVEL transmembrane domain-containing 3 (CMTM3) has been identified in a number of human tumors and tumor cell lines, including gastric and testicular cancer, and PC3, CAL27 and Tca-83 cell lines. However, the association between CMTM3 expression and the clinicopathological features and prognosis of esophageal squamous cell carcinoma (ESCC) patients remains unclear. The aim of the present study was to investigate the correlation between CMTM3 expression and clinicopathological parameters and prognosis in ESCC. CMTM3 mRNA and protein expression was analyzed in ESCC and paired non-tumor tissues by quantitative real-time polymerase chain reaction, western blotting and immunohistochemical analysis. The Kaplan-Meier method was used to plot survival curves and the Cox proportional hazards regression model was also used for univariate and multivariate survival analysis. The results revealed that CMTM3 mRNA and protein expression levels were lower in 82.5% (30/40) and 75% (30/40) of ESCC tissues, respectively, when compared with matched non-tumor tissues. Statistical analysis demonstrated that CMTM3 expression was significantly correlated with lymph node metastasis (P=0.002) and clinical stage (P<0.001) in ESCC tissues. Furthermore, the survival time of ESCC patients exhibiting low CMTM3 expression was significantly shorter than that of ESCC patients exhibiting high CMTM3 expression (P=0.01). In addition, Kaplan-Meier survival analysis revealed that the overall survival time of patients exhibiting low CMTM3 expression was significantly decreased compared with patients exhibiting high CMTM3 expression (P=0.010). Cox multivariate analysis indicated that CMTM3 protein expression was an independent prognostic predictor for ESCC after resection. This study indicated that CMTM3 expression is significantly decreased in ESCC tissues and CMTM3 protein expression in resected tumors may present an effective prognostic biomarker.

The tumor-suppressive role of BATF2 in esophageal squamous cell carcinoma.

BATF2 has been found to be decreased in a variety of human malignancies, while its clinical significance and functional roles in esophageal squamous cell carcinoma (ESCC) remain unknown. Herein, the aim of this study was to investigate the expression pattern and to explore the potential functions of BATF2 in ESCC tissues and cell lines. BATF2 mRNA and protein expression levels in human tissues and human ESCC cell lines were evaluated by quantitative real­time polymerase chain reaction (qRT-PCR), western blotting (WB) and immunohistochemical (IHC) analyses. BATF2 was upregulated by transfection of the pcDNA3.1­BATF2 plasmid into KYSE-410 cells. MTT and Transwell assays were used to investigate the effects of BATF2 on cellular proliferation and invasion. Survival curves were plotted using Kaplan-Meier plots and log-rank tests. Cox's proportional hazards regression model was used to analyze univariate and multivariate survival. The results showed that, compared to the matched non-tumor tissues from 36 ESCC patients, 80.56% (29/36) of the tumor tissues presented downregulation of BATF2 by WB analysis (P<0.001). The results of IHC in 104 patients who underwent surgery for ESCC showed that the expression of BATF2 was closely related to tumor differentiation (P=0.023) and lymph node metastasis (P=0.027), while there was no significant correlation with age (P=0.574), gender (P=0.357), tumor location (P=0.721) and TNM stage (P=0.126) of the patients. Pathological grade (P=0.027), clinical stage (P=0.000), lymph node metastasis (P=0.002) and BATF2 expression (P=0.028) were identified as independent prognostic factors for overall survival (OS). In the in vitro studies, upregulation of BATF2 expression significantly inhibited the proliferation and invasive ability of the human ESCC KYSE-410 cells. In conclusion, as a tumor suppressor, BATF2 serves as a prognostic biomarker of ESCC and it may be a potential therapeutic target for ESCC treatment.