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Changsha, China

Xie B.,8th Changsha Hospital | Xie B.,Central South University | Chen J.,8th Changsha Hospital | Liu B.,8th Changsha Hospital | Zhan J.,Central South University
Pathology and Oncology Research | Year: 2013

The klotho gene is a classical "aging suppressor" gene. Its roles in the pathology of chronic kidney diseases have been well documented. However, the role of Klotho in tumorigenesis, cancer progression, and prognosis is attracting more and more attention. Recent studies have shown that Klotho participates in the progression of several types of human cancers. Klotho functions as a tumor suppressor by inhibiting insulin/IGF1, p53/p21, and Wnt signaling. Silencing klotho gene expression is mainly mediated through promoter hypermethylation and histone deacetylation in cancer. Klotho has been proposed to take part in cell proliferation, survival, autophagy, and resistance to anti-cancer therapies. © 2013 Arányi Lajos Foundation. Source


Liu T.,Central South University | Yu X.,8th Changsha Hospital | Zhang X.,Central South University | Li Z.,Central South University | Zeng W.,Central South University
Turkish Journal of Medical Sciences | Year: 2012

Aim: To evaluate the results of the management of post-traumatic tibial infected nonunion using bone transport with external fixators. Materials and methods: We retrospectively reviewed a consecutive series of 35 patients from 2000 to 2008 in our hospital who were treated for the post-traumatic tibial nonunion by bone transport with an external fixator. Thirty-two limbs (80%) were in active infected state. The mean amount of bone defect was 3.5 cm (range 1.0 to 7.8 cm) as measured on plain radiographs. The mean leg-length discrepancy was 4.4 cm (range 0 to 8.7 cm). Results: The mean follow-up was 72.5 months (range 35-106 months). All the patients had bony union and the infection had been controlled. The mean external fixation index was 40.7 day/cm (range 34.2-46.9 day/cm). The mean length gained was 7.9 cm (range 4.0-10.5 cm). Based on the criteria recommended by Paley et al., 28 bone results were excellent, 5 good, 2 fair, and none poor;30 functional results were excellent, 4 good, 1 fair, and none poor. Conclusion: Bone transport with an external fixator is a safe, effective, and minimally invasive technique to treat posttraumatic tibial infected nonunion. © TÜBITAK. Source


Xie B.,Central South University | Zhou J.,Central South University | Shu G.,Central South University | Liu D.-C.,Central South University | And 2 more authors.
Cancer Cell International | Year: 2013

Background: The loss of tumor suppressor gene expression is involved in the carcinogenesis of gastric cancer (GC). Klotho is a recently identified tumor suppressor gene that epigenetically inactivated in gastric cancer. However, the signaling pathways involved in the suppressive role of klotho have rarely been reported in gastric cancer. In this study, we investigated the involvement of klotho in gastric cancer cell proliferation, apoptosis, and autophagy as well as the associated signaling. Methods: Methylation of klotho gene promoter in GC-7901, MNK-45 and AGS gastric cancer cells as well as GES-1 normal gastric epithelial cells was detected by bisulfate-based PCR. Restoration of klotho gene expression was established by applying a demethylating agent and delivering aklotho gene expression vector into GC-7901 cells. Cell viability was measured by CCK-8 assay. Cell apoptosis and cycling were analyzed by flow cytometry. Autophagy was measured by detecting LC3-I and LC3-II expression. Protein levels and phosphorylation were measured by Western blot assay. Results: Methylation of klotho gene promoter and expression of the klotho gene were detected in GC cells. Restoration of klotho gene expression significantly inhibited cell proliferation, induced cell apoptosis, and increased LC3-I/LC3-II expression in GC cells. Restoration of klotho gene expression downregulated the phosphorylation levels of IGF-1 receptor, IRS-1, PI3K, Akt, and mTOR proteins. Both apoptosis and autophagy inhibitors blocked klotho-induced apoptosis and autophagy. Conclusion: Klotho is a tumor suppressor in gastric cancer, which regulates IGF-1R phosphorylation and the subsequent activation of IRS-1/PI3K/Akt/mTOR signaling, tumor cell proliferation, apoptosis, and autophagy. © 2013 Xie et al; licensee BioMed Central Ltd. Source


Shu G.,Central South University | Xie B.,Central South University | Ren F.,Central South University | Liu D.-C.,Central South University | And 4 more authors.
Cellular Oncology | Year: 2013

Purpose: Klotho has been identified as a tumor suppressor in several human malignancies including hepatocellular carcinoma (HCC). However, the signaling pathways involved in the tumor suppressive role of klotho in HCC have not been reported. Here, we investigated the role of klotho in HCC cell proliferation, apoptosis, autophagy, and invasion, as well as its associated signal transduction pathways. Methods: Restoration of klotho gene expression was established by delivering a klotho gene expression vector into the human HCC cell lines HepG2 and MHCC-97-H. Cell viability was measured using a cell counting (CCK-8) assay and apoptosis was analyzed through flow cytometry. Autophagy was measured via LC3-I and LC3-II protein expression levels and tumor cell invasion was assessed using a Matrigel invasion chamber assay. Expression and phosphorylation of several apoptosis and survival related proteins were assessed using Western blot assays. Results: Exogenous klotho gene expression significantly inhibited HCC cell proliferation, induced HCC cell apoptosis, increased LC3-I and LC3-II protein expression in HCC cells, and decreased migration of HCC cells in a Matrigel invasion chamber assay. Exogenous klotho gene expression also down-regulated the phosphorylation levels of the IGF-1 receptor, and the downstream Akt, ERK, and p70S6K proteins. Both apoptosis and autophagy inhibitors decreased klotho-induced apoptosis and autophagy. Conclusion: Klotho is a tumor suppressor that, through the regulation of IGF-1R phosphorylation and subsequent activation of downstream Akt-p70S6K and ERK signaling, regulates HCC tumor cell proliferation, apoptosis, autophagy and invasion. © 2012 International Society for Cellular Oncology. Source

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