Mechanism underlying tumorigenesis induced by Bcr-Abl oncogene and A-MuLV virus.

Yanan Sun; Na Chen; Xuefei Wang; Ji-long Chen; Yanmei MA

Return

Mechanism underlying tumorigenesis induced by Bcr-Abl oncogene and A-MuLV virus.

Author: Yanan SUN ¹ ; Na CHEN ¹ ; Xuefei WANG ² ; Ji-Long CHEN ¹ ; Yanmei MA ¹
Author Information

1. State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, China.
2. CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China.
Publication Type:Journal Article
Keywords: A-MuLV; Bcr-Abl; cancer; lncRNA; signalling pathway; tyrosine kinase
MeSH: Abelson murine leukemia virus; Animals; Cell Transformation, Neoplastic; Fusion Proteins, bcr-abl; Genes, abl; Humans; Phosphatidylinositol 3-Kinases
From: Chinese Journal of Biotechnology 2018;34(12):1943-1952
CountryChina
Language:Chinese
Abstract: The Bcr-Abl oncogene is produced by the reciprocal translocation between c-Abl gene on chromosome 9 and the Bcr gene on chromosome 22 in human genome. The encoded Bcr-Abl fusion protein is responsible for the pathogenesis of certain human leukemias. Abelson murine leukemia virus (A-MuLV) is a retrovirus that could lead to transformation of B lymphocyte in mice, and v-Abl is the oncogene of A-MuLV. Abl oncoproteins (such as Bcr-Abl and v-Abl) play critical roles in tumorigenesis of certain cell types. Several signal transduction pathways, including JAK/STAT/Pim, PI3K/AKT/mTOR and RAS/RAF/MEK signaling pathway, are involved in Abl-mediated tumorigenesis. In addition, Abl-mediated tumorigenesis is associated with mutation or abnormal modification of key signal molecules as well as dysregulation of some critical long noncoding RNAs (lncRNAs). Here, we review the molecular mechanisms by which Abl oncogenes activate three major signaling pathways, and provide a scientific basis for therapy of Abl oncoprotein-induced tumors.