IGFBP6 Regulates Cell Apoptosis and Migration in Glioma

Bei, Yuanqi; Huang, Qiyu; Shen, Jianhong; Shi, Jinlong; Shen, Chaoyan; Xu, Peng; Chang, Hao; Xia, Xiaojie; Xu, Li; Ji, Bin; Chen, Jianguo

doi:10.1007/s10571-016-0426-4

Cited by 20 publications

(12 citation statements)

References 27 publications

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“…IGFBP1 binds to and prolongs the serum half-life of IGF2 and both it and IGF2BP-3, which binds to and stabilizes IGF2 mRNA, have been reported to drive cancer growth and to be associated in some cases with an adverse prognosis (96). In contrast, IGFBP5 and IGFBP7, which were down-regulated in HCCs by 5-fold and 2-fold, respectively, are negative regulators of IGF2 and thus possess potential tumor suppressor functions (97)(98)(99). These findings, together with the 25-fold down-regulation of IGF1 transcripts (Supplemental Table S4), support the idea that HCC tumor growth is at least supported by, if not entirely dependent upon, complex and coordinate activities of members of the H19-IGF2 axis.…”

Section: Discussionmentioning

confidence: 99%

Sequential adaptive changes in a c-Myc-driven model of hepatocellular carcinoma

Dolezal¹,

Wang²,

Kulkarni³

et al. 2017

Journal of Biological Chemistry

168

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Hepatocellular carcinoma (HCC) is a common cancer that frequently overexpresses the c-Myc (Myc) oncoprotein. Using a mouse model of Myc-induced HCC, we studied the metabolic, biochemical, and molecular changes accompanying HCC progression, regression, and recurrence. These involved altered rates of pyruvate and fatty acid β-oxidation and the likely re-directing of glutamine into biosynthetic rather than energy-generating pathways. Initial tumors also showed reduced mitochondrial mass and differential contributions of electron transport chain complexes I and II to respiration. The uncoupling of complex II's electron transport function from its succinate dehydrogenase activity also suggested a mechanism by which Myc generates reactive oxygen species. RNA sequence studies revealed an orderly progression of transcriptional changes involving pathways pertinent to DNA damage repair, cell cycle progression, insulin-like growth factor signaling, innate immunity, and further metabolic re-programming. Only a subset of functions deregulated in initial tumors was similarly deregulated in recurrent tumors thereby indicating that the latter can "normalize" some behaviors to suit their needs. An interactive and freely available software tool was developed to allow continued analyses of these and other transcriptional profiles. Collectively, these studies define the metabolic, biochemical, and molecular events accompanyingHCCevolution, regression, and recurrence in the absence of any potentially confounding therapies.

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Section: Discussionmentioning

confidence: 99%

Sequential adaptive changes in a c-Myc-driven model of hepatocellular carcinoma

Dolezal¹,

Wang²,

Kulkarni³

et al. 2017

Journal of Biological Chemistry

168

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“…IGFBP6 encourages migration in rhabdomyosarcoma cells via mediating the MAP kinase signaling pathway [53], while IGFBP6 plays a suppressive role on tumor growth in ACTH-secreting pituitary adenoma through activation of the PI3K-AKT-mTOR signaling pathway [54]. In addition, IGFBP6 is inversely associated with glioma grade and predicts better survival [55]. The low expression of IGFBP6 is related to poor clinical outcomes and unfavorable prognosis in gastric adenocarcinoma [56].…”

Section: Discussionmentioning

confidence: 99%

The Prognostic Values of the Insulin‐Like Growth Factor Binding Protein Family in Ovarian Cancer

Zheng

Chen

Xia

et al. 2020

BioMed Research International

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Purpose. To assess the expression of insulin-like growth factor binding protein (IGFBP) family and its prognostic impact in ovarian cancer (OC) patients. Materials and Methods. The mRNA expression and protein expression of individual IGFBPs in healthy ovarian samples and OC tissues were explored through Oncomine, Gene Expression Profiling Interactive Analysis, and Human Protein Atlas database. Additionally, the prognostic values of the six IGFBP members in patients with OC were evaluated by Kaplan-Meier plotter. Results. IGFBP2 and IGFBP4 mRNA expression were remarkably upregulated in patients with OC. To be specific, the mRNA expression of IGFBP2 was upregulated in patients with serous ovarian cancer (SOC), while IGFBP1/3/4/5/6 mRNA levels were downregulated. In addition, the IGFBP4 protein expression was upregulated in SOC, and the IGFBP6 protein expression was upregulated in both of SOC and endometrioid ovarian cancer (EOC) tissues. High IGFBP1 mRNA levels showed favorable overall survival (OS) and progression-free survival (PFS) in all OC. Meanwhile, increased IGFBP5/6 mRNA levels revealed worsen OS and PFS in all OC patients. IGFBP4/6 mRNA levels predicted unfavorable OS and PFS only in SOC patients. Moreover, the aberrant mRNA expression of IGFBP1/2/4/5/6 was correlated with significantly prognosis in patients receiving different chemotherapeutic regimens. Conclusion. This study indicates that the IGFBP family reveals distinct prognosis in patients with OC. IGFBP1/2/4/5/6 are useful prognostic predictors for chemotherapeutic effect in OC patients, and IGFBP2/4 are potential tumor markers for the diagnosis of OC.

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“…Nell-1 is a secreted molecule that can induce cranial suture bone growth [26, 27]. However, higher levels of expressions of GRIAL1, SGOL1 and Igfbp6 were found within parietal bone that displayed anti-proliferative feature, such as overexpression of GRIAL1 is anti-proliferative [28], and SGOL1 and Igfbp6 are involved in cell apoptosis [29-31]. Foxp2 can increase cell differentiation without affecting cell proliferation and cell survival [32], and transient upregulation of Foxp2 in pre-osteoblast mesenchymal cells regulates a p21-dependent growth arrest checkpoint [33].…”

Section: Discussionmentioning

confidence: 99%

Physiological Signatures of Dual Embryonic Origins in Mouse Skull Vault

Zhao

et al. 2017

Cell Physiol Biochem

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Background/Aims: The mammalian skull vault is a highly regulated structure and consists of several membrane bones of different tissue origins (e.g. neural crest derived frontal bone and mesoderm derived parietal bone). Although membrane bones form through intramembranous ossification, neural crest derived frontal bone has superior osteoblast activity and bone regeneration ability, triggering a novel conception for craniofacial reconstruction and bone regeneration called endogenous calvarial regeneration. However, a comprehensive landscape of the genes and signaling pathways involved in this process is not clear. Methods: Transcriptome analysis within the two bone elements is firstly performed to determine the physiological signatures of differential gene expressions in mouse skull vault. Results: Frontal bone tissues and parietal bone tissues maintain tissue origin through special gene expression similar to neural crest vs mesoderm tissue, and physiological functions between these two tissues are also found in differences related to proliferation, differentiation and extracellular matrix production and clustered signaling pathways. Conclusion: Our data provide novel insights into the potential gene regulatory network in regulating the development of neural crest-derived frontal bone and mesoderm-derived parietal bone.

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IGFBP6 Regulates Cell Apoptosis and Migration in Glioma

Cited by 20 publications

References 27 publications

Sequential adaptive changes in a c-Myc-driven model of hepatocellular carcinoma

Sequential adaptive changes in a c-Myc-driven model of hepatocellular carcinoma

The Prognostic Values of the Insulin‐Like Growth Factor Binding Protein Family in Ovarian Cancer

Physiological Signatures of Dual Embryonic Origins in Mouse Skull Vault

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