Institute of Pathology and Pathophysiology

Shenyang, China

Institute of Pathology and Pathophysiology

Shenyang, China
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Deng X.,Institute of Pathology and Pathophysiology | Wang E.-H.,Institute of Pathology and Pathophysiology | Cui C.,Liaoning Medical University | Li G.-S.,Liaoning Medical University | Yu B.-Z.,Institute of Pathology and Pathophysiology
Cell Proliferation | Year: 2011

Objectives: Proline-rich inositol polyphosphate 5-phosphatase (PIPP) is one of the signal-modifying enzymes that play pivotal regulatory roles in PI3K signalling pathway. The aim of this study was to determine the role of PIPP in early development of fertilized mouse eggs, via inhibition of Akt activity and subsequent downstream signalling events. Materials and methods: The mRNA transcript levels of endogenous PIPP and Akt1, Akt2, Akt3 were detected in G 1, S, G 2 and M phases of fertilized mouse eggs by RT-PCR. Levels of exogenous PIPP, phosphorylated Akt at Ser473, dephosphorylated cdc2 at Tyr15 and levels of CCNB1, were detected respectively by immunoblotting. Changes in Akt localization were observed by fluoroimmunoassay; meanwhile, changes in activity of Akt and its downstream MPF were detected. Percentages of cells undergoing division were determined by counting, using a dissecting microscope. Results: PIPP and Akt1 transcripts were detectable in G 1, S, G 2 and M phases of fertilized mouse eggs, but Akt2 and Akt3 were not. We also observed that overexpression of PIPP in fertilized eggs decreased expression of phosphorylated Akt at Ser473 and altered membrane localization of phosphorylated Akt at Ser473 specifically. Furthermore, overexpression of PIPP resulted in decreases in mitosis-phase promoting factor activity, level of dephosphorylated cdc2 at Tyr15 and cleavage rate of fertilized mouse eggs. Conclusions: Our data suggest, for the first time, that PIPP may affect development of fertilized mouse eggs by inhibition of level of phosphorylated Akt at Ser473 and subsequent inhibition of downstream signal cascades. © 2011 Blackwell Publishing Ltd.

Xiu Y.-L.,Shenyang University | Zhao Y.,Shenyang University | Gou W.-F.,Institute of Pathology and Pathophysiology | Chen S.,Shenyang University | And 2 more authors.
PLoS ONE | Year: 2014

Background: Anacardic acid (AA) is a mixture of 2-hydroxy-6-alkylbenzoic acid homologs. Certain antitumor activities of AA have been reported in a variety of cancers. However, the function of AA in ovarian cancer, to date, has remained unknown. Methods: Ovarian cancer cell lines were exposed to AA, after which cell proliferation, apoptosis, invasion and migration assays were performed. Phalloidin staining was used to observe lamellipodia formation. Reverse transcription polymerase chain reaction (RT-PCR) and western blotting were used to assess the mRNA and protein expression levels of Phosphatidylinositol 3-kinase (PI3K), vascular endothelial growth factor (VEGF) and caspase 3. Results: Our results showed that AA promotes ovarian cancer cell proliferation, inhibits late apoptosis, and induces cell migration and invasion, as well as lamellipodia formation. AA exposure significantly up-regulated PI3K and VEGF mRNA and protein expression, while, in contrast, it down-regulated caspase 3 mRNA and protein expression in comparison to untreated control cells. Conclusion: Taken together, our results demonstrate for the first time that AA may potentiate the proliferation, invasion, metastasis and lamellipodia formation in ovarian cancer cell lines via PI3K, VEGF and caspase 3 pathways. © 2014 Xiu et al.

Dai S.-D.,Shenyang Medical College | Dai S.-D.,Institute of Pathology and Pathophysiology | Wang Y.,Shenyang Medical College | Wang Y.,Institute of Pathology and Pathophysiology | And 16 more authors.
Cancer Science | Year: 2011

δ-Catenin is the only member of the p120 catenin (p120ctn) subfamily that its primary expression is restricted to the brain. Since δ-catenin is upregulated in human lung cancer, the effects of δ-catenin overexpression in lung cancer still need to be clarified. Immunohistochemistry was performed to investigate the expression of δ-catenin and Kaiso, a δ-catenin-binding transcription factor, in 151 lung cancer specimens. A correlation between cytoplasmic δ-catenin and Kaiso expression was also associated with high TNM stage, lymph node metastases and poor prognosis. Co-immunoprecipitation assay confirmed the interactions of δ-catenin and Kaiso in lung cancer cells. In addition, gene transfection and RNAi technology were used to demonstrate that increased δ-catenin expression was promoted, whereas its knockdown suppressed its lung cancer invasive ability. In addition, methylation-specific PCR and ChIP assay demonstrated that δ-catenin could regulate MTA2 via Kaiso in a methylation-dependent manner, while it could regulate cyclin D1 and MMP7 expression through Kaiso in a sequence-specific manner. In conclusion, a δ-catenin/Kaiso pathway exists in lung cancer cells. Increased δ-catenin expression is critical for maintenance of the malignant phenotype of lung cancer, making δ-catenin a candidate target protein for future cancer therapeutics. © 2010 Japanese Cancer Association.

Tian X.,Shenyang University | Dai S.,Shenyang Medical College | Dai S.,Institute of Pathology and Pathophysiology | Sun J.,Liaoning Cancer Hospital and Institute | And 6 more authors.
Oncotarget | Year: 2015

Kruppel-like factor 4 (KLF4), a member of the KLF family of transcription factors, has been considered as a crucial tumor suppressor in hepatocellular carcinoma (HCC). Using affinity purifications and mass spectrometry, we identified FBXO22, Cullin1 and SKP1 as interacting proteins of KLF4. We demonstrate that F-box only protein 22 (FBXO22) interacts with and thereby destabilizes KLF4 via polyubiquitination. As a result, FBXO22 could promote HCC cells proliferation both in vitro and in vivo. However, KLF4 deficiency largely blocked the proliferative roles of FBXO22. Importantly, FBXO22 expression was markedly increased in human HCC tissues, which was correlated with down-regulation of KLF4. Therefore, our results suggest that FBXO22 might be a major regulator of HCC development through direct degradation of KLF4.

Tian X.,Shenyang University | Dai S.,Shenyang Medical College | Dai S.,Institute of Pathology and Pathophysiology | Sun J.,Liaoning Cancer Hospital and Institute | And 9 more authors.
Evidence-based Complementary and Alternative Medicine | Year: 2015

Bufalin, a digoxin-like active component of the traditional Chinese medicine Chan Su, exhibits potent antitumor activities in many human cancers. Bufalin induces mitochondria-dependent apoptosis in cancer cells, but the detailed molecular mechanisms are largely unknown. hTERT, the catalytic subunit of telomerase, protects against mitochondrial damage by binding to mitochondrial DNA and reducing mitochondrial ROS production. In the present study, we investigated the effects of bufalin on the cell viability, ROS production, DNA damage, and apoptosis of CAPAN-2 human pancreatic and CAL-27 human oral cancer cells. Bufalin reduced CAPAN-2 and CAL-27 cell viability with IC50 values of 159.2 nM and 122.6 nM, respectively. The reduced cell viability was accompanied by increased ROS production, DNA damage, and apoptosis and decreased expression of hTERT. hTERT silencing in CAPAN-2 and CAL-27 cells by siRNA resulted in increased caspase-9/-3 cleavage and DNA damage and decreased cell viability. Collectively, these data suggest that bufalin downregulates hTERT to induce mitochondria-dependent apoptosis in CAPAN-2 and CAL-27 cells. Moreover, bufalin increased the phosphorylation of JNK and p38-MAPK in CAPAN-2 and CAL-27 cells, and blocking the JNK/p38-MAPK pathway using the JNK inhibitor SP600125 or the p38-MAPK inhibitor SB203580 reversed bufalin-induced hTERT downregulation. Thus, the JNK/p38 pathway is involved in bufalin-induced hTERT downregulation and subsequent induction of apoptosis by the mitochondrial pathway. © 2015 Xin Tian et al.

PubMed | Institute of Pathology and Pathophysiology
Type: | Journal: OncoTargets and therapy | Year: 2013

The present study was designed to determine whether Allium ursinum L (ramson) could inhibit the proliferation of human AGS gastric cancer cells. Furthermore, we attempted to determine whether this inhibition could occur by targeting regulatory elements of the cell cycle.Flow cytometry was used to observe apoptosis and the cell cycle in AGS cell lines treated or not treated with ramson watery extract. Proteins related to the cell cycle were detected by Western blotting. Caspase activity was measured using a colorimetric assay kit according to the manufacturers instructions.Ramson watery extract induced apoptosis and G2/M phase arrest in AGS cells. Western blotting showed that cyclin B was inhibited by ramson watery extract. However, G1 phase-related proteins remain unchanged after treatment.Our results indicate that ramson effectively sup pressed proliferation and induced apoptosis and G2/M arrest in AGS cells by regulating elements of the cell cycle.

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