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Shao J.-L.,Peoples Hospital of Gaoyou | Hu G.-X.,Peking University | Zheng J.,Peking University | Wan Z.-Y.,Jiangxi Provincial Chest Hospital | Jiang R.-J.,Peoples Hospital of Zhaoxian
Academic Journal of Second Military Medical University | Year: 2014

Objective To observe the effects of hydroxycamptothecin (HCPT) on hepatic expression of Bax, Bcl-2 genes, and crsmooth muscle actin (α-SMA) and hepatic fibrosis in rats. Methods Sixty-four SDrats were randomly divided into 5 groups: normal control group, model group, low-dose HCPT group, intermediate-dose HCPT group and high-dose HCPT group. Hepatic fibrosiswas induced in rats by abdominal injection of CC14- The normal control group was injected with normal saline only; the low-dose, intermediate-dose, and high-dose groups were injected with HCPT (3 times a week for 8 weeks) at 0. 25, 0. 5 and 1. 0 mg/kg, respectively. At the end of the 8th week, liver tissues were obtained from each group for H-E staining and Masson staining to observe the degree of hepatic fibrosis. The expression of Bax, Bel-2 mRNA and the Bax/ Bel-2 mRNA ratio in liver tissues were examined by RT-PCR. Immunohistochemical staining was used to observe crSMA protein expression and TUNEL staining wasused to observe cell apoptosis. Results Notable hepatic fibrosis was found in model group (HI stage in2rats, II stage in8 rats). Compared with the model group, each HCPT group had significantly improved fibrosis (P<0. 05; low-doseHCPT group: E stage in 1, H stage in 8, II stage in 1; intermediate-doseHCPT group: E stage in 7, H stage in 3; and high-dose HCPT group: E stage in 1, H stage in 7, II stage in 2). RT-PCR results showed that the expression of Bax and Bel-2 mRNA in the model group was significantly higher than that in the normal control group (P< 0. 05), and the expression in the three HCPT groups were significantly lower than that in the model group (P<0. 05), with the ratio of Bax/Bcl-2 mRNA in the model group being significantly lower than those in the three HCPT groups (all P<0. 05). The immunohistochemistry result showed that the hepatic α-SMA level in the model group was significantly higher than those in the intermediate- and high-dose HCPT groups (P<0. 05). The TUNELstaining showedno significantly positive staining in the normal control group ormodel group, and positive staining in all the three HCPT groups. Conclusion HCPT has protective effect on CC14-induced hepatic fibrosis in rats; inhibiting proliferation of hepatic stellate cells, up-regulating Bax/Bcl-2 mRNA ratio might be part of the related mechanism. Source


Ling D.-J.,Ministry of Health Hepatobiliary and Enteric Surgery Center | Chen Z.-S.,Ministry of Health Hepatobiliary and Enteric Surgery Center | Zhang Y.-D.,Ministry of Health Hepatobiliary and Enteric Surgery Center | Liao Q.-D.,Central South University | And 3 more authors.
Molecular Medicine Reports | Year: 2015

Previous studies have identified a variety of microRNAs (miRNAs) that have important roles in cancer progression, particularly in tumor invasion and metastasis. Downregulation of miR-145 was reported to occur in various types of human cancer; however, the role of miR-145 in lung cancer metastasis and its potential mechanisms of action remain to be elucidated. The present study aimed to investigate the effects of miR-145 on metastasis and epithelial-mesenchymal transition (EMT) in A549 human lung adenocarcinoma cells. In addition, the underlying mechanisms by which miR-145 regulates EMT were examined. The miR-145 mimic was transfected into A549 cells; cell invasion and adhesion assays were then performed in order to investigate cell metastasis, and western blot analysis was used to examine the expression of EMT markers. In order to further examine the underlying mechanisms by which miR-145 regulates EMT, a luciferase reporter assay was performed to determine whether miR-145 targeted Oct4. In addition, the expression of Wnt3a and β-catenin in A549 cells was measured following transfection with small hairpin RNA-Oct4. To the best of our knowledge, the results of the present study demonstrated for the first time, that miR-145 inhibited lung cancer cell metastasis and EMT via targeting the Oct4 mediated Wnt/β-catenin signaling pathway. Source


Ling D.-J.,Central South University | Chen Z.-S.,Central South University | Liao Q.-D.,Central South University | Feng J.-X.,Jiangxi Provincial Chest Hospital | And 2 more authors.
Experimental and Therapeutic Medicine | Year: 2016

Non-small cell lung cancer (NSCLC) accounts for >80% of all cases of lung cancer and can be divided into lung adenocarcinoma (LAC), large-cell carcinoma (LCC), and squamous cell carcinoma (SCC). Accumulating evidence suggests that MTSS1, which is a newly discovered protein associated with tumor progression and metastasis, may have differential roles in cancer malignancy. As it has been demonstrated that MTSS1 is overexpressed in NSCLC and may be an independent prognostic factor in patients with SCC, the present study explored the differential roles of MTSS1 in the invasion and proliferation of different subtypes of NSCLC. Stable overexpression and knockdown of MTSS1 was performed in human NSCLC H920 (LAC), H1581 (LCC) and SW900 cell lines (SCC), and western blot, cell invasion, proliferation and FAK activity analyses were used to investigate the effects. Overexpression of MTSS1 enhanced the invasion and proliferation abilities of H920 and H1581 cells, and these effects were abolished by treatment with selective FAK inhibitor 14, which did not affect the expression of MTSS1. Notably, overexpression of MTSS1 inhibited invasion and proliferation in SW900 cells, and this effect was enhanced by the selective FAK inhibitor. Knockdown of MTSS1 decreased the invasion and proliferation abilities of H920 and H1581 cells, whereas knockdown increased invasion and proliferation in SW900 cells. Furthermore, while overexpression of MTSS1 induced FAK phosphorylation and activity in H920 and H1581 cells, MTSS1 overexpression inhibited FAK phosphorylation/activity in SW900 cells. Knockdown of MTSS1 decreased FAK phosphorylation/activity in H920 and H1581 cells, whereas knockdown increased these processes in SW900 cells. To the best of our knowledge, the present study was the first to demonstrate that MTSS1 has differential roles in various subtypes of NSCLC, acting via a FAK-dependent mechanism. The results indicated that MTSS1 may enhance invasion and proliferation in LAC and LCC cells, whereas MTS11 inhibits these processes in SCC cells. These findings provide novel insight into the functional role of MTSS1 in cancer and may help elucidate therapeutic strategies for the treatment of various types of cancer. © 2016, Spandidos Publications. All rights reserved. Source


Chen Z.-S.,Central South University | Ling D.-J.,Central South University | Zhang Y.-D.,Central South University | Feng J.-X.,Jiangxi Provincial Chest Hospital | And 2 more authors.
Molecular Medicine Reports | Year: 2015

Clinical studies have reported evidence for the involvement of octamer-binding protein 4 (Oct4) in the tumorigenicity and progression of lung cancer; however, the role of Oct4 in lung cancer cell biology in vitro and its mechanism of action remain to be elucidated. Mortality among lung cancer patients is more frequently due to metastasis rather than their primary tumors. Epithelial-mesenchymal transition (EMT) is a prominent biological event for the induction of epithelial cancer metastasis. The aim of the present study was to investigate whether Oct4 had the capacity to induce lung cancer cell metastasis via the promoting the EMT in vitro. Moreover, the effect of Oct4 on the β-catenin/E-cadherin complex, associated with EMT, was examined using immunofluorescence and immunoprecipitation assays as well as western blot analysis. The results demonstrated that Oct4 enhanced cell invasion and adhesion accompanied by the downregulation of epithelial marker cytokeratin, and upregulation of the mesenchymal markers vimentin and N-cadherin. Furthermore, Oct4 induced EMT of lung cancer cells by promoting β-catenin/E-cadherin complex degradation and regulating nuclear localization of β-catenin. In conclusion, the present study indicated that Oct4 affected the cell biology of lung cancer cells in vitro through promoting lung cancer cell metastasis via EMT; in addition, the results suggested that the association and degradation of the β-catenin/E-cadherin complex was regulated by Oct4 during the process of EMT. Source


Wang C.-W.,Jiangxi Provincial Chest Hospital | Yu S.-L.,Jiangxi Provincial Chest Hospital | Liu Y.-J.,Jiangxi Provincial Chest Hospital | Xiong G.-L.,Jiangxi Provincial Chest Hospital
Chinese Journal of Cancer Prevention and Treatment | Year: 2014

OBJECTIVE: To investigate the clinical significance of neutrophil gelatinase-associated lipocalin (NGAL) in non-small cell lung cancer through the detection of expression levels in cancer and adjacent tissues.METHODS: The expression levels of NGAL mRNA and portion in 65 patients with NSCLC (35 cases of squamous cell carcinoma and 30 cases of adenocarcinoma) at the Chest Hospital of jiangxi were detected by real-time PCR and immunohistochemical techniques. The adjacent normal tissues were detected by the same methods as control. The relationships between NGAL protein expression and the clinical data were analyzed.RESULTS: The real-time PCR study demonstrated that the difference of ΔCt between NGAL mRNA in adenocarcinomas and β-actin in squamous carcinoma were -2.3±1.2 and -2.8±1.5 respectively. Both of them were higher than that in the adjacent group (P〈0.05). and the positive rates of NGAL protein in three groups were 80.0% (24/30), 57.1 (20/35) and 32.3 (21/65) (P〈0.05). NGAL expression was not associated with gender, age, smoking history, lymph node metastasis in NSCLC patients (P〉0.05).CONCLUSIONS: Based on these findings, the expression of NGAL is increased in NSCLC and related with the NSCLC typing. It may be an important tumor marker to predict NSCLC. ©, 2014, Chinese Journal of Cancer Prevention and Treatment, Editorial board. All right reserved. Source

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