High Expression of ABL2 Suppresses Apoptosis in Gastric Cancer

Dig Dis Sci. 2018 Sep;63(9):2294-2300. doi: 10.1007/s10620-018-5111-7. Epub 2018 May 16.

Abstract

Background: Diseases associated with Abelson-related gene (also called ABL2) include leukemia; furthermore, previous researches have studied the expressions and functions of ABL2 in different types of malignancies and found that it plays an important role in almost all kinds of cancers.

Aims: Nevertheless, the mechanism of ABL2 in gastric cancer (GC) remains vague.

Methods: In the present study, the level of ABL2 in human GC tissues was detected by immunohistochemistry. Also, the GC cell lines MGC-803 and BGC-823 were selected to stably knock down and overexpress the level of ABL2 by corresponding lentiviral vectors. Puromycin was used to maintain the stable low expression of ABL2 MGC-803 cells compared with control cells; what is more, the high expression of ABL2 BGC-823 cells was also obtained. Based on it, we detected the proteins associated with apoptosis, such as Bcl-2 family and caspase family by western blotting.

Results: The most appropriate concentration of puromycin to kill GC cells is 1 µg/mL; then, we obtained the corresponding stable cell lines. Furthermore, we found that high level of ABL2 in BGC-823 cells increased the expression of Bcl-XL, total PARP, and caspase3, while decreased the level of cleaved caspase3 and cleaved caspase9. Consistent results are received in MGC-803 cells. In addition, ABL2 overexpression led to the protein related with Ras/Erk and PI3K/AKT signaling pathway increased; also, we found that the major proteins play a significant role in it.

Conclusion: All the data showed that high expression of ABL2 suppresses apoptosis through Ras/Erk and PI3K/AKT signaling pathway in GC cell lines.

Keywords: ABL2; Apoptosis; Bcl-XL; Caspase; Gastric cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Apoptosis / physiology*
  • Cell Line, Tumor
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Protein-Tyrosine Kinases / biosynthesis*
  • Protein-Tyrosine Kinases / genetics*
  • Stomach Neoplasms / genetics*
  • Stomach Neoplasms / metabolism*
  • Stomach Neoplasms / pathology

Substances

  • ARG tyrosine kinase
  • Protein-Tyrosine Kinases