Primary structure of human insulin-like growth factor II.
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Amino Acid Sequence↗
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Results for “Insulin-Like Growth Factor II”
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Insulin-like growth factors I and II: some biological actions and receptor binding characteristics of two purified constituents of nonsuppressible insulin-like activity of human serum.
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Adipose Tissue↗
Multiplication stimulating activity regulates ornithine decarboxylase in isolated porcine granulosa cells in vitro.
The polypeptide growth factor, multiplication stimulating activity (MSA), stimulates ornithine decarboxylase (ODC) activity in isolated porcine granulosa cells maintained under chemically defined conditions in vitro. The stimulatory action of MSA is saturable, and dose-dependent (0.1-1000 ng/ml). MSA effects are additive to those of luteinizing hormone (LH), but not those of follicle stimulating hormone (FSH). Stimulation of ODC activity by MSA requires cellular protein and RNA synthesis, and appears to be mediated independently of cyclic AMP. These observations provide the first demonstration of MSA action in the mammalian ovary.
Amanitins↗
Epigenomic profiling links IGF2 overexpression to anthracycline resistance in colorectal cancer organoids.
This study provides evidence of a new treatment approach for colorectal peritoneal metastases, a condition associated with a worse prognosis than other types of metastases.
Humans↗
Comparison of [125I]somatomedin A and [125I]somatomedin C radioreceptor assays for somatomedin peptide content in whole and acid-chromatographed plasma.
The placental membrane radioreceptor assay was used to measure the levels of somatomedin (SM) peptides in plasma. Displacement of both [125I]somatomedin A ([125I]SM-A) and [125I]somatomedin C ([125I]SM-C) by normal whole plasma, the peptide fraction of acid-chromatographed plasma, and a partially purified, insulin-free SM preparation were compared. The peptide fraction of plasma was isolated by acid chromatography over Sephadex G-50 in 0.25 M formic acid with a yield of greater than or equal to 90%, as determined by bioassay and [125I]SM. In the case of [125I]SM-A, the dose-response curves for whole plasma, acid-chromatographed plasma, and the standard SM preparation were parallel (P less than 0.2). In contrast, for [125I]SM-C, the dose-response curves for acid-chromatographed plasma and the purified SM preparation were parallel (P less than 0.2), but both differed significantly from that of whole plasma (P less than 0.001). In addition, there was less variability in the assay of acid-chromatographed plasma compared to whole plasma. The results indicate that radioreceptor assay of unextracted normal plasma using [125I]SM-A is a valid measure of SM peptide concentration, while radioreceptor assay of unextracted normal plasma using [125I]SM-C, in our hands, is not. Acid chromatography of plasma before its assay is an uncomplicated procedure which allows valid and precise measurement of SM peptide content using either [125I]SM-A or [125I]SM-C.
Adult↗
The genetic changes in 11p15.5-related pheochromocytomas and paragangliomas.
Pheochromocytomas and paragangliomas (PPGLs) are neuroendocrine tumors. The development of these tumors is associated with more than 20 genes. The aforementioned genes are subdivided into three clusters. The pseudohypoxic, kinase-signaling and Wnt clusters. The pseudohypoxic cluster is the only one that has been demonstrated to be associated with DNA methylation changes, including alterations in the 11p15.5 region. The objective of this study was to identify alterations in the 11p15.5 region, ascertain their prevalence in PPGLs, and subsequently compare them with the genomic and somatic mutations that cluster PPGLs. One hundred and fifty tumor samples were subjected to analysis. A total of 90 cases (60%) exhibited no alterations in the 11p15.5 region. The most prevalent alterations were maternal allele loss, observed in 45 cases (30%), pUPD (paternal uniparental disomy) in five cases (3.33%), and paternal allele gain in four cases (2.67%). The data presented here suggest that two mechanisms may be involved in the formation of PPGLs. These are reduced expression of CDKN1C (maternal allele deletion) and overexpression of IGF2 (pUPD, paternal allele gain). A statistically significant difference was observed in the frequency of alterations in the 11p15.5 region when comparing cluster 1 and cluster 2 (P-value <0.0001). This study is the first to describe pUPD and paternal allele gain as somatic alterations in PPGLs. In addition, our findings indicate that alterations in the 11p15.5 region are not exclusive to cluster 1. Consequently, the alterations in the 11p15.5 region cannot be regarded as a marker for cluster 1.
Humans↗
Convergent IGF2 overexpression in pheochromocytoma/paraganglioma: insights from Beckwith-Wiedemann syndrome.
Beckwith-Wiedemann syndrome (BWS) is an imprinting disorder characterized by overgrowth and tumor predisposition, caused by dysregulated expression of genes on chromosome 11p15.5. An association between BWS and pheochromocytoma/paraganglioma (PPGL) has been suggested in isolated case reports over the past fifty years, but the molecular basis for this link remains unclear. We identified four patients with BWS who developed metastatic PPGL and investigated IGF2 pathway activation in these tumors and in PPGL across various genotypes. Pan-cancer transcriptomic analysis of The Cancer Genome Atlas (TCGA) demonstrated that PPGL overexpresses IGF2, with pseudohypoxic tumors exhibiting higher expression compared to other molecular clusters. Loss of heterozygosity and loss of imprinting at 11p15.5 partially explain this overexpression, with PPGL additionally demonstrating globally elevated expression of imprinted genes compared to most other tumor types, suggesting a broader relaxation of genomic imprinting. Cognate receptor profiling revealed that PPGLs are equipped to respond to IGF2 signaling, with high expression of IGF1R and insulin receptor isoform A (IR-A). Immunohistochemistry confirmed IGF2 protein overexpression in both BWS-associated and genotypically diverse sporadic PPGLs. Our results indicate that IGF2 overexpression is a convergent molecular feature of PPGL across genotypes and suggest the IGF2 pathway as a potential diagnostic and therapeutic target.
Humans↗
The influence of early nutrition on growth and the circulating levels of immunoreactive somatomedin A.
The effect of nutrition during early development on growth and serum immunoreactive somatomedin A was examined in rats by rearing in small or large liters. At weaning, body weight, brain weight, liver weight and DNA content was significantly reduced in rats whose nutrition was restricted by rearing in large litters. Brain DNA content was significantly altered. Serum somatomedin A was significantly reduced in the growth-retarded rats as compared to those whose growth was enhanced by rearing in small litters. Similarly, maternal serum somatomedin A was significantly reduced in rats nursing large litters.
Animals↗
Nonsuppressible insulin-like activity and thyroid hormones: major pituitary-dependent sulfation factors for chick embryo cartilage.
Serum from hypothyroid hypophysectomized rats did not stimulate sulfation or incorporation of amino acids into chick embryo sterna. When such rats were treated for a short time with growth hormone (somatotropin), their serum stimulated incorporation both of sulfate and of amino acids. The different actions of the two types of sera were not due to changes in thyroid state. The results support the existence in serum of a sulfation factor for chick embryo cartilage that is dependent upon growth hormone. Highly purified preparations of nonsuppressible insulin-like activity from human serum stimulated incorporation of amino acids, and of uridine into RNA, in chick embryo sterna in vitro; chondrocytes prepared from this tissue had specific high-affinity binding sites for this insulin-like activity. However, sulfate incorporation was stimulated very little, unless serum from hypothyroid hypophysectomized rats was also present. When L-3,5,3'-triiodothyronine was added as well, the stimulation was enhanced further. From these and other experiments, we conclude that (i) nonsuppressible insulin-like activity or a closely related peptide is the growth-hormone-dependent growth and sulfation factor for chick embryo cartilage: (ii) a second, unidentified factor must be present for the insulin-like activity to stimulate sulfation; and (iii) stimulation of sulfation by thyroid hormones in vitro is additive to that of nonsuppressible insulin-like activity.
Animals↗
Gene model for the ortholog of Ilp4 in Drosophila eugracilis.
Gene Model for Insulin-like peptide 4 (Ilp4) in the D. eugracilis (DeugGB2) assembly (GCA_000236325.2). The characterization of this ortholog was carried out as part of a larger, ongoing dataset designed to explore the evolution of the insulin/insulin-like growth factor signaling (IIS) pathway across the genus Drosophila, utilizing the Genomics Education Partnership gene annotation protocol within Course-based Undergraduate Research Experiences.
Bioinformatics↗
Gene Model for the ortholog of Ilp2 in Drosophila ananassae.
Gene model for the ortholog of Insulin-like peptide 2 ( Ilp2 ) in the D. ananassae May 2011 (Agencourt dana_caf1/DanaCAF1) Genome Assembly (GenBank Accession: GCA_000005115.1 ) of Drosophila ananassae . This ortholog was characterized as part of a developing dataset to study the evolution of the Insulin/insulin-like growth factor signaling pathway (IIS) across the genus Drosophila using the Genomics Education Partnership gene annotation protocol for Course-based Undergraduate Research Experiences.
Journal Article↗
Metabolic Dysfunction-Associated Carcinogenesis: Molecular Mechanisms and the Preventive Roles of Phytochemicals Part I: Pathophysiological Mechanisms Linking Metabolic Dysfunction to Cancer.
The global cancer burden is projected to escalate to 27 million new cases annually by 2040, a trajectory that parallels the rising prevalence of obesity, metabolic dysfunction, and related metabolic disorders. While genetic and environmental factors are well-recognized, the systemic metabolic environment is increasingly identified as a critical determinant of tumorigenesis. This review (Part I) systematically delineates the molecular and cellular framework through which metabolic dysfunction orchestrates a tumor-permissive landscape. We evaluate six primary pathophysiological axes: (1) chronic low-grade inflammation that fuels a protumorigenic milieu, (2) oxidative stress and redox imbalance leading to genomic instability, (3) insulin resistance and insulin-like growth factor axis activation which stimulate mitogenic pathways, (4) aberrant lipid metabolism and lipotoxicity-driven cell transformation, (5) gut microbiota dysbiosis and its modulation of the tumor microenvironment, and (6) metabolism-associated epigenetic remodeling that sustains oncogenic gene expression. Unlike previous literature that has focused on isolated pathways, this synthesis emphasizes the synergistic crosstalk among these mechanisms, illustrating how they collectively reinforce cancer initiation and progression. Furthermore, this mechanistic framework provides a biological rationale for targeting metabolism-associated carcinogenesis through dietary phytochemicals and bioactive compounds, which will be comprehensively discussed in Part II. By providing an integrated overview of the metabolic dysfunction-cancer axis, this work establishes a mechanistic foundation for the preventive potential of phytochemicals. These insights are crucial for developing multitarget dietary strategies against metabolism-associated malignancies.
carcinogenesis↗
Amino-terminal sequences of two polypeptides from human serum with nonsuppressible insulin-like and cell-growth-promoting activities: evidence for structural homology with insulin B chain.
The amino-terminal sequences of two polypeptides with nonsuppressible insulin-like and cell-growth-promoting activities (NSILA I and II), isolated from human serum, were determined. Of the first 31 residues, 22 are identical in NSILA I and II. Moreover, a striking structural similarity was found between NSILA and insulin B chain: 47 and 57% of residues 1-30 in NSILA I are identical to those in insulin B chain from man and tuna fish, respectively. This high degree of sequence identity is presented as evidence for homology and thus for a common evolutionary origin of insulin and NSILA. Based on these results and on these results and on biological properties of NSILA described earlier, a new designation for NSILA is proposed: insulin-like growth factor (IGF).
Amino Acid Sequence↗