Release date: 2018-02-09
Studies reveal the molecular mechanisms of tumorigenesis caused by Rheb mutations
Recently, the disease genomics research team led by Liu Yang, a researcher at the Biotechnology Translation Medical Science Center of the Dalian Institute of Chemical Physics of the Chinese Academy of Sciences, has made new progress in the field of tumor transformation medicine. The team first revealed the molecular mechanisms underlying the development and progression of renal and cervical cancer driven by mutations in the Rheb gene and provided new clinical strategies and methods that could potentially be used to treat Rheb mutant tumors. Related results were published in Oncogene magazine.
The TSC/mTOR signaling pathway is an important signaling pathway regulating biological activities such as cell survival, metabolism, proliferation and autophagy. In many tumors, abnormal activation of this signaling pathway leads to overexpression of proteins associated with tumor proliferation. Recent tumor-wide genome sequencing results indicate that there is a higher frequency of Rheb-Y35N site mutations in cervical cancer and renal cancer, but the molecular mechanism of tumorigenesis caused by this gene mutation is still unclear. In response to this problem, the team demonstrated through a series of cell-level and mouse models that the mutation can cause sustained activation of the MAPK signaling pathway, thereby promoting tumor cell proliferation and survival. Synergistic inhibition of MAPK and mTOR signaling pathways can effectively inhibit Rheb-Y35N-induced tumor cell growth.
The research team also cooperated with the research team of Li Guohui and combined with structural biology and molecular biology research methods to further prove that the Rheb-Y35N mutant can bind to the kinase domain of AMPKα1, thereby competitively inhibiting the wild-type Rheb. Activation of the AMPK signaling pathway in the absence of nutrient deficiencies, thereby attenuating the phosphorylation of AMPK to the inhibitory phosphorylation of S729 at BRAF, ultimately leading to sustained activation of the MEK-ERK signal.
The results of this study not only found the molecular mechanism of tumorigenesis caused by Rheb mutation, but also provided a new clinical basis and theoretical basis for the treatment of tumors driven by Rheb-Y35N.
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Source: Dalian Institute of Chemical Physics
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