Tags

Type your tag names separated by a space and hit enter

Helicobacter pylori infection of gastric cancer cells elevates the level of expression and activation of protein kinase D2.
Exp Oncol. 2009 Sep; 31(3):134-9.EO

Abstract

AIM

To test the hypothesis, whether H. pylori infection may affect the level of PKD2 expression and/or activation in gastric cancer cells.

METHODS

Studies were performed on AGS human gastric adenocarcinoma cell line, gastric tissues samples from 36 cases of different histological variants of gastric cancer. Immunohistochemical, cell and molecular biology, bacteriological and biochemical approaches have been used in this study.

RESULTS

H. pylori 16S rRNA gene was detected in 97% cases of gastric tumors, and in 83% of cases csmall a, CyrillicgA gene was detected. In all tested adenocarcinoma samples cagA+ H. pylori was revealed. These cases were characterized by high level of PKD1/2 expression and autophosphorylation. In adenogenic cancer samples the presence of cagA- H. pylori was identified. Carcinoid and nondifferentiated gastric cancers contain H. pylori, with very low numbers of cagA+ copies. All cases of gastric tumors with cagA- H. pylori had very low levels of PKD1/2 autophosphorylation. AGS cell line infection with cagA- and cagA+ H. small er, Cyrillicylori resulted in elevation of PKD2 expression levels in 3.29 and 3.66 times respectively (p < 0.001). In cells infected by cag+ H. small er, Cyrillicylori the level of PKD2 transphosphorylation was 1.39 higher than in cells infected by cagA- H. pylori. For PKD2 autophosphorylation this difference was even higher - 3.27 times (p < 0.001).

CONCLUSION

H. pylori infection enhanced the level of protein kinase D2 expression, trans- and autophosphorylation. The level of PKD2 autophosphorylation/activation was higher in AGS cell line inoculated of with cag+ H. pylori than in AGS cells with cagA- H. pylori. These suggest that H. pylori induces activation of PKD1/2 and could exploit PKD2 mediated signaling pathways that may contribute to the pathogenesis of gastric cancer.

Authors+Show Affiliations

Institute of Experimental Pathology, Oncology and Radiobiology, NAS of Ukraine, Kiev, Ukraine.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19783969

Citation

Shabelnik, M Yu, et al. "Helicobacter Pylori Infection of Gastric Cancer Cells Elevates the Level of Expression and Activation of Protein Kinase D2." Experimental Oncology, vol. 31, no. 3, 2009, pp. 134-9.
Shabelnik MY, Kostyuk OV, Merentsev SV, et al. Helicobacter pylori infection of gastric cancer cells elevates the level of expression and activation of protein kinase D2. Exp Oncol. 2009;31(3):134-9.
Shabelnik, M. Y., Kostyuk, O. V., Merentsev, S. V., Tarasova, T. O., & Sidorenko, S. P. (2009). Helicobacter pylori infection of gastric cancer cells elevates the level of expression and activation of protein kinase D2. Experimental Oncology, 31(3), 134-9.
Shabelnik MY, et al. Helicobacter Pylori Infection of Gastric Cancer Cells Elevates the Level of Expression and Activation of Protein Kinase D2. Exp Oncol. 2009;31(3):134-9. PubMed PMID: 19783969.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Helicobacter pylori infection of gastric cancer cells elevates the level of expression and activation of protein kinase D2. AU - Shabelnik,M Yu, AU - Kostyuk,O V, AU - Merentsev,S V, AU - Tarasova,T O, AU - Sidorenko,S P, PY - 2009/9/29/entrez PY - 2009/9/29/pubmed PY - 2009/12/16/medline SP - 134 EP - 9 JF - Experimental oncology JO - Exp Oncol VL - 31 IS - 3 N2 - AIM: To test the hypothesis, whether H. pylori infection may affect the level of PKD2 expression and/or activation in gastric cancer cells. METHODS: Studies were performed on AGS human gastric adenocarcinoma cell line, gastric tissues samples from 36 cases of different histological variants of gastric cancer. Immunohistochemical, cell and molecular biology, bacteriological and biochemical approaches have been used in this study. RESULTS: H. pylori 16S rRNA gene was detected in 97% cases of gastric tumors, and in 83% of cases csmall a, CyrillicgA gene was detected. In all tested adenocarcinoma samples cagA+ H. pylori was revealed. These cases were characterized by high level of PKD1/2 expression and autophosphorylation. In adenogenic cancer samples the presence of cagA- H. pylori was identified. Carcinoid and nondifferentiated gastric cancers contain H. pylori, with very low numbers of cagA+ copies. All cases of gastric tumors with cagA- H. pylori had very low levels of PKD1/2 autophosphorylation. AGS cell line infection with cagA- and cagA+ H. small er, Cyrillicylori resulted in elevation of PKD2 expression levels in 3.29 and 3.66 times respectively (p < 0.001). In cells infected by cag+ H. small er, Cyrillicylori the level of PKD2 transphosphorylation was 1.39 higher than in cells infected by cagA- H. pylori. For PKD2 autophosphorylation this difference was even higher - 3.27 times (p < 0.001). CONCLUSION: H. pylori infection enhanced the level of protein kinase D2 expression, trans- and autophosphorylation. The level of PKD2 autophosphorylation/activation was higher in AGS cell line inoculated of with cag+ H. pylori than in AGS cells with cagA- H. pylori. These suggest that H. pylori induces activation of PKD1/2 and could exploit PKD2 mediated signaling pathways that may contribute to the pathogenesis of gastric cancer. SN - 1812-9269 UR - https://www.unboundmedicine.com/medline/citation/19783969/Helicobacter_pylori_infection_of_gastric_cancer_cells_elevates_the_level_of_expression_and_activation_of_protein_kinase_D2_ L2 - https://medlineplus.gov/helicobacterpyloriinfections.html DB - PRIME DP - Unbound Medicine ER -