[Show abstract][Hide abstract] ABSTRACT: Phospho-PRAS40(Thr246) (phosphorylated proline-rich Akt substrate of 40 kilodaltons at Thr246) is a biomarker for phosphatidylinositol 3-kinase (PI3K) pathway activation and AKT inhibitors sensitivity.
In this study, we immunohistochemically investigated the expression of phospho-PRAS40(Thr246) in 141 gastric cancer tumors, and evaluated its clinicopathological and prognostic significance.
Sixty-four cases (45.4%) were defined as phospho-PRAS40(Thr246) positive. Phospho-PRAS40(Thr246) correlated positively with lymph node metastasis, lymphatic infiltration, vascular infiltration and shorter survival. Furthermore, phospho-PRAS40(Thr246) is an independent prognostic factor for gastric cancer.
Our data suggest that phospho-PRAS40(Thr246) was frequently expressed in gastric cancers, and correlated with malignant progression and poor prognosis of patients. PI3K pathway-targeted therapies should be considered in the future treatment of gastric cancers.
Archives of Medical Science 02/2014; 10(1):149-53. DOI:10.5114/aoms.2013.36927 · 2.03 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The study investigated the extraction process of active ingredients from akebia stem and an analysis of their anti-gastric cancer activity. Three different extraction methods were used to obtain extracts, namely the decoction method (group A), reflux extraction method (group B), and maceration method (group C), of which reflux extraction method and maceration method used ethanol as the extraction solvent, while decoction method used distilled water for extraction. The differences in anti-gastric cancer activity of the three extracts were compared. MTT assay was used to test and compare the inhibitory effects of extracts obtained in A, B, and C groups on gastric cancer cells. The results showed that the dry extract obtained by heat reflux extraction with "water-ethanol" ratio of 1:2, extractant volume of 70 ml, with ethanol as extraction solvent presented the best inhibitory activity on gastric cancer SGC-7901 cells in this study. Its inhibitory effect did not change over time, and was directly proportional to the concentration.
African Journal of Traditional, Complementary and Alternative Medicines 12/2013; 10(5):313-7. · 0.56 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Introduction:
Up to present, EGF 61*A/G, TGF-β1 -509*T/C and TNF-α -308*A/G gene polymorphisms have been analysed in other cancer entities than hepatocellular carcinoma (HCC). We here investigated the frequency of these gene polymorphisms among HCC patients.
Materials and methods:
A total of 73 HCC patients and 117 cancer-free healthy people were recruited at the Surgical Department of Zhongshan Hospital. Genomic DNA was isolated from peripheral blood and gene polymorphisms were analyzed by PCR-RFLP.
The distribution of EGF 61*G/G homozygotes among HCC patients was more frequent than that in the control group (24.7% vs 11.1%, OR=2.618, 95%CI=1.195-5.738). In parallel, the frequency of the "G" allele in the HCC patient group was also higher than that in the control group (45.9% vs 33.3%, OR= 1.696, 95%CI=1.110-2.592). No difference could be found for the TGF-β1-509 and TNF-α -308 genotypes.
EGF 61*G/G genotype and G allele are significantly increased among patients with HCC. TGF-β1-509*T/C and TNF-α -308*A/G gene polymorphisms are not related to this cancer entity.
Asian Pacific journal of cancer prevention: APJCP 12/2012; 13(12):6217-20. DOI:10.7314/APJCP.2012.13.12.6217 · 2.51 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Recently, population-based studies of type 2 diabetes patients have provided evidence that metformin treatment is associated with a reduced cancer incidence and mortality, but its mode of action remains unclear. Here we report effects of metformin on hepatocellular carcinoma (HCC) Hep-G2 cells and details of molecular mechanisms of metformin activity. Our research indicates that metformin displays anticancer activity against HCC through inhibition of the mTOR translational pathway in an AMPK-independent manner, leading to G1 arrest in the cell-cycle and subsequent cell apoptosis through the mitochondrion-dependent pathway. Furthermore, we showed that metformin strongly attenuated colony formation and dramatically inhibited Hep-G2 tumor growth in vivo. In conclusion, our studies suggested that metformin might have potential as a cytotoxic drug in the prevention and treatment of HCC.
Asian Pacific journal of cancer prevention: APJCP 07/2012; 13(7):3275-9. DOI:10.7314/APJCP.2012.13.7.3275 · 2.51 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: P21-activated protein kinase (Pak1), a main downstream effector of small Rho GTPases, plays an important role in the regulation of cell morphogenesis, motility, mitosis and angiogenesis. However, the role of Pak1 in gastric cancer metastasis remains unclear. Here, we showed that Pak1 is overexpressed in gastric cancer tissues from 74 patients by immunohistochemistry. Overexpression of Pak1 was associated with metastasis and prognosis of gastric cancer. In addition, overexpression of Pak1 increased gastric cancer cell motility and invasion, whereas downregulation of Pak1 expression reduced gastric cancer cell migration and invasion. In further study, data showed that activated Pak1 inhibited stress fiber and focal adhesion complex formation in gastric cancer cells and led to the formation of motile phenotypes. Importantly, activated Pak1 elicited phosphorylation of the ERK and JNK-dependent pathway in gastric cancer cell lines. In conclusion, our results suggest that Pak1 is overexpressed in gastric cancer and plays an important role in the metastasis of gastric cancer. The mechanism by which Pak1 induces cancer metastasis may involve activation of ERK and JNK.