Insulin-Like Growth Factor 1 (IGF-1) Signaling in Glucose Metabolism in Colorectal Cancer

Kasprzak, Aldona

doi:10.3390/ijms22126434

Cited by 54 publications

(30 citation statements)

References 277 publications

(448 reference statements)

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“…IGF-1, IGFBP, and IGF-1R have been considered as important regulators in glucose metabolic homeostasis [ 20 , 21 ]. In our study, intestinal IGF-1 and IGFBP-3 were elevated by 72.7% and 77.4% in diabetic mice compared to control ( Figure 5 A–C), and berberine treatment decreased intestinal IGF-1, IGFBP-3, and IGF-1/IGFBP-3 level by84.8%, 35.2%, and 76.6% ( Figure 5 A–C).…”

Section: Resultsmentioning

confidence: 99%

Berberine Decreases Intestinal GLUT2 Translocation and Reduces Intestinal Glucose Absorption in Mice

Zhang

Yang

et al. 2021

IJMS

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Postprandial hyperglycemia is an important causative factor of type 2 diabetes mellitus, and permanent localization of intestinal GLUT2 in the brush border membrane is an important reason of postprandial hyperglycemia. Berberine, a small molecule derived from Coptidis rhizome, has been found to be potent at lowering blood glucose, but how berberine lowers postprandial blood glucose is still elusive. Here, we investigated the effect of berberine on intestinal glucose transporter 2 (GLUT2) translocation and intestinal glucose absorption in type 2 diabetes mouse model. Type 2 diabetes was induced by feeding of a high-fat diet and injection of streptozotocin and diabetic mice were treated with berberine for 6 weeks. The effects of berberine on intestinal glucose transport and GLUT2 translocation were accessed in isolated intestines and intestinal epithelial cells (IEC-6), respectively. We found that berberine treatment improved glucose tolerance and systemic insulin sensitivity in diabetic mice. Furthermore, berberine decreased intestinal glucose transport and inhibited GLUT2 translocation from cytoplasm to brush border membrane in intestinal epithelial cells. Mechanistically, berberine inhibited intestinal insulin-like growth factor 1 (IGF-1R) phosphorylation and thus reduced localization of PLC-β2 in the membrane, leading to decreased GLUT2 translocation. These results suggest that berberine reduces intestinal glucose absorption through inhibiting IGF-1R-PLC-β2-GLUT2 signal pathway.

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“…IGF-1, as a PI3K agonist, is frequently used to verify the mechanism of the PI3K/Akt pathway [ 62 – 64 ]. The biological function of IGF-I is mainly mediated by IGF-I receptor.…”

Section: Discussionmentioning

confidence: 99%

Manual Acupuncture at ST37 Modulates TRPV1 in Rats with Acute Visceral Hyperalgesia via Phosphatidylinositol 3-Kinase/Akt Pathway

Chen

Dong

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Acupuncture can significantly ameliorate inflammatory pain in acute visceral hyperalgesia. Hyperalgesia is attenuated by inflammatory mediators that activate transient receptor potential vanilloid 1 (TRPV1), and TRPV1 is regulated by nerve growth factor (NGF)-induced phosphatidylinositol 3-kinase (PI3K)/Akt pathway. However, it is unknown whether NGF-induced PI3K/Akt pathway is associated with manual acupuncture (MA). In this study, the effect and mechanism of MA at Shangjuxu (ST37) and Quchi (LI11) were examined using an acetic acid-induced rat model with visceral hyperalgesia. We demonstrated that MA at ST37 significantly decreased abdominal withdrawal reflex (AWR) scores, proinflammatory cytokine expression (TNF-α, IL-1β, and IL-6), and TRPV1 protein and mRNA expression in rats with acute visceral hyperalgesia compared with the untreated controls, while MA at LI11 showed no effect. The effects of MA at ST37 were reversed after treatment with the PI3K agonist IGF-1 30 min before MA. In rats with visceral hyperalgesia, the upregulation of NGF, tropomyosin-receptor-kinase A (TrkA), PI3K, and phosphorylation-Akt (p-Akt) was decreased by MA at ST37, indicating that TRPV1 regulation via the NGF-induced PI3K/Akt pathway plays a vital role in the effects of MA-mediated amelioration of acute visceral hyperalgesia.

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“…with a higher glycolytic rate than HKI( Tan and Miyamoto 2015 ). HKIV, also known as glucokinase, is present in hepatocytes with the lowest affinity for glucose and no inhibition by G6P ( Xu and Herschman 2019 ; Kasprzak 2021 ). HKII is essential for tumor metabolism.…”

Section: Glucose Metabolism In Neoplastic Cellsmentioning

confidence: 99%

Noncoding RNAs in the Glycolysis of Ovarian Cancer

Zhang

Liu

2022

Front. Pharmacol.

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Energy metabolism reprogramming is the characteristic feature of tumors. The tumorigenesis, metastasis, and drug resistance of ovarian cancer (OC) is dependent on energy metabolism. Even under adequate oxygen conditions, OC cells tend to convert glucose to lactate, and glycolysis can rapidly produce ATP to meet their metabolic energy needs. Non-coding RNAs (ncRNAs) interact directly with DNA, RNA, and proteins to function as an essential regulatory in gene expression and tumor pathology. Studies have shown that ncRNAs regulate the process of glycolysis by interacting with the predominant glycolysis enzyme and cellular signaling pathway, participating in tumorigenesis and progression. This review summarizes the mechanism of ncRNAs regulation in glycolysis in OC and investigates potential therapeutic targets.

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“…The conversion brings PI3-kinase dependent kinase-2 (PDK2) and AKT Serine/Threonine Kinase (Akt) to the membrane and the phosphorylation of Akt activates a number of substrates to regulate protein synthesis, cell proliferation, apoptosis and other cellular activities (Bikle et al, 2015;Yoshida and Delafontaine, 2020;Moonesi et al, 2021). IGF1 can also activate the Grb2 adaptor protein and inducts the activation of Ras G protein to initiate the mitogen-activated kinase (MAPK) pathway, which involves Ras, Raf, MEK and ERK signaling molecules (Clemmons, 2006;Kasprzak, 2021).…”

Section: Igf Signalingmentioning

confidence: 99%

IGF Signaling in Intervertebral Disc Health and Disease

Lin

Tian

Peng

et al. 2022

Front. Cell Dev. Biol.

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Low back pain (LBP) is a common musculoskeletal symptom, which brings a lot of pain and economic loss to patients. One of the most common causes of LBP is intervertebral disc degeneration (IVDD). However, pathogenesis is still debated, and therapeutic options are limited. Insulin-like growth factor (IGF) signaling pathways play an important role in regulating different cell processes, including proliferation, differentiation, migration, or cell death, which are critical to the homeostasis of tissues and organs. The IGF signaling is crucial in the occurrence and progression of IVDD. The activation of IGF signaling retards IVDD by increasing cell proliferation, promoting extracellular matrix (ECM) synthesis, inhibiting ECM decomposition, and preventing apoptosis and senescence of disc cells. However, abnormal activation of IGF signaling may promote the process of IVDD. IGF signaling is currently considered to have a promising treatment prospect for IVDD. An in-depth understanding of the role of IGF signaling in IVDD may help find a novel approach for IVDD treatment.

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“…The GH/ IGF1 axis and IGF system contribute to promote colorectal tumorigenesis through different mechanisms: deregulating Wnt/b-catenin signaling (39)(40)(41), reducing the responsiveness of cells to Transforming Growth Factor Beta (TGFb) (42), enhancing the anti-apoptotic effects of both Cyclooxygenase-2 (Cox-2) (43) and Bcl2 Like 1 (Bcl-X L) (44), and enhancing the expression of the pro-angiogenetic Vascular Endothelial Growth Factor (VEGF) (45,46). Moreover, a recent review extensively discussed the role of the activation of PI3K/AKT/mTOR Complex (mTORC) signaling pathway, and Raf/MAPK signaling pathway in the increased glucose uptake and aerobic glycolysis (Warburg effect) by CRC cells (47).…”

Section: Mirnas and Lncrnas Regulating The Gh/igf1 Axis And Igf System In Cancer: Focus On Pituitary Adenoma Osteosarcoma And Colorectal mentioning

confidence: 99%

GH and IGF System: The Regulatory Role of miRNAs and lncRNAs in Cancer

et al. 2021

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Growth hormone (GH) and the insulin-like growth factor (IGF) system are involved in many biological processes and have growth-promoting actions regulating cell proliferation, differentiation, apoptosis and angiogenesis. A recent chapter in epigenetics is represented by microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) which regulate gene expression. Dysregulated miRNAs and lncRNAs have been associated with several diseases including cancer. Herein we report the most recent findings concerning miRNAs and lncRNAs regulating GH and the IGF system in the context of pituitary adenomas, osteosarcoma and colorectal cancer, shedding light on new possible therapeutic targets. Pituitary adenomas are increasingly common intracranial tumors and somatotroph adenomas determine supra-physiological GH secretion and cause acromegaly. Osteosarcoma is the most frequent bone tumor in children and adolescents and was reported in adults who were treated with GH in childhood. Colorectal cancer is the third cancer in the world and has a higher prevalence in acromegalic patients.

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Insulin-Like Growth Factor 1 (IGF-1) Signaling in Glucose Metabolism in Colorectal Cancer

Cited by 54 publications

References 277 publications

Berberine Decreases Intestinal GLUT2 Translocation and Reduces Intestinal Glucose Absorption in Mice

Manual Acupuncture at ST37 Modulates TRPV1 in Rats with Acute Visceral Hyperalgesia via Phosphatidylinositol 3-Kinase/Akt Pathway

Noncoding RNAs in the Glycolysis of Ovarian Cancer

IGF Signaling in Intervertebral Disc Health and Disease

GH and IGF System: The Regulatory Role of miRNAs and lncRNAs in Cancer

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