Abstract
Simple SummaryGlioblastoma multiforme (GBM) is a serious and aggressive cancer disease that has not allowed scientists to rest for decades. In this review, we consider the new gene pair |-SRGAP2–FAM72-| and discuss its role in the cell cycle and the possibility of defining new therapeutic approaches for the treatment of GBM and other cancers via this gene pair |-SRGAP2–FAM72-|.Neural stem cells (NSCs) offer great potential for regenerative medicine due to their excellent ability to differentiate into various specialized cell types of the brain. In the central nervous system (CNS), NSC renewal and differentiation are under strict control by the regulation of the pivotal SLIT-ROBO Rho GTPase activating protein 2 (SRGAP2)—Family with sequence similarity 72 (FAM72) master gene (i.e., |-SRGAP2–FAM72-|) via a divergent gene transcription activation mechanism. If the gene transcription control unit (i.e., the intergenic region of the two sub-gene units, SRGAP2 and FAM72) gets out of control, NSCs may transform into cancer stem cells and generate brain tumor cells responsible for brain cancer such as glioblastoma multiforme (GBM). Here, we discuss the surveillance of this |-SRGAP2–FAM72-| master gene and its role in GBM, and also in light of FAM72 for diagnosing various types of cancers outside of the CNS.
Highlights
Introduction published maps and institutional affilThe human brain is a unique organ that can perform higher cognitive functions and is different from all other species
Some studies showed that retinoblastoma transcriptional corepressor 1 (RB1) may cause the cell to go into the G0 phase with different cell fates: Quiescent G0 with reversible return option to reenter the cell cycle for proliferation, post-mitotic G0 with irreversible cell differentiation, or cell senescence G0, eventually leading to apoptosis [41,42]
Demethylation (5hmC) is significantly increased when Neural stem cells (NSCs) and neural progenitor cells (NPGs) differentiate into neurons [141]. This is in contrast to the hypomethylation observed during oncogenesis in Family with sequence similarity 72 (FAM72) or the lack of methylation changes observed in SLIT-ROBO Rho GTPase activating protein 2 (SRGAP2), confirming that the proliferative and neurogenic mechanisms occur via completely different mechanisms under normal and pathophysiological conditions in the |-SRGAP2–FAM72-| master gene
Summary
Our understanding of the molecular mechanism driving ACC has advanced. Alterations in the components of the WNT1/β-catenin, EGFR, and TP53 pathways are prominent markers in ACC [29,30,31,32]. We identified a complex novel ACC-specific gene signature: CRIPAK, DGKZ, GARS1, LRIG1, ZFPM1, and ZNF517, which was significantly, and most repeatedly mutated in ACC and correlated with high FAM72 expression (Figure 3) [28]. This gene set is involved in tumor suppression and cellular proliferation and could be useful for the prognosis and development of therapeutic approaches for the treatment of ACC. E; CENPF, Centromere protein F; CEP55, Centrosomal protein 55; CRIPAK, Cysteine-rich p21-activated protein kinase 1 inhibitor; CTNNB1, Catenin beta 1; DGKZ, Diacylglycerol kinase zeta; FZD, Frizzleds; GARS1, Glycyl-tRNA synthetase 1; KIF14/23, Kinesin family member 14/23; LRIG1, Leucine rich repeats and immunoglobulin-like domains 1; NEK2, Never in mitosis gene a-related kinase 2; NUF2, NUF2 component of NDC80 kinetochore complex; RPL22, Ribosomal protein L22; PRKAR1A, Protein kinase cAMP-dependent type I regulatory subunit alpha; RAS, Rat sarcoma; SGO1, Shugoshin 1; WNT1, Wingless and Int-1 family member 1; ZFPM1, Zinc finger protein, friend of GATA family member 1; ZNF517, Zinc finger protein 517; ZNRF3, Zinc and ring finger 3
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