High Expression of ABL2 Suppresses Apoptosis in Gastric Cancer
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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.
Nevertheless, the mechanism of ABL2 in gastric cancer (GC) remains vague.
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.
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.
All the data showed that high expression of ABL2 suppresses apoptosis through Ras/Erk and PI3K/AKT signaling pathway in GC cell lines.
KeywordsABL2 Apoptosis Gastric cancer Caspase Bcl-XL
This work was founded by the National Natural Science Foundation of China (Grant No. 81772157), Natural Science Foundation of Jiangsu Province, China (Grant No. BK20161345), Key Young Medicine Talents of Jiangsu Province (Grant No. QNRC2016457), and Major Program of Natural Science Research in Colleges and Universities of Jiangsu Province in 2017 (Grant No. 17KJA320001).
Compliance with ethical standards
Conflict of interest
The authors have no conflict of interest to declare.
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