Insulin-like growth factor 1 regulates the location, stability, and transcriptional activity of β-catenin

Playford, Martin P.; Bicknell, David; Bodmer, W F; Macaulay, Valentine M.

doi:10.1073/pnas.210394297

Cited by 256 publications

(183 citation statements)

References 62 publications

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“…Bcr-Abl can phosphorylate b-catenin, which inhibits its association with Axin/GSK-3b complex and reduces its phosphorylation by GSK-3b and subsequent proteosomal degradation (Coluccia et al, 2007). IGF-1R activation also Autocrine IGF-1 signaling in CML A Lakshmikuttyamma et al leads to b-catenin phosphorylation, stabilization and nuclear localization (Playford et al, 2000;Chen et al, 2005). Thus, IGF-1 signaling may be responsible for b-catenin stability or it may cooperate with Bcr-Abl to further enhance b-catenin stability.…”

Section: Discussionmentioning

confidence: 99%

Bcr-Abl induces autocrine IGF-1 signaling

et al. 2008

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Section: Discussionmentioning

confidence: 99%

Bcr-Abl induces autocrine IGF-1 signaling

et al. 2008

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“…In addition to playing a role in cell proliferation (31,32), neuropeptides and other regulatory peptides may have a possible effect on the control of adhesion between neighboring epithelial cells (33) and on catenin regulation, which is a crucial process related to colonic carcinogenesis (34). Interestingly, it has been observed that adherens junctions and tight junctions are regulated by gastrin in epithelial cells, a fact that may contribute to the co-carcinogenic role of this prohormone in colorectal carcinoma (35).…”

Section: Discussionmentioning

confidence: 99%

Intrinsic denervation of the colon is associated with a decrease of some colonic preneoplastic markers in rats treated with a chemical carcinogen

Vespúcio

Turatti

Modiano

et al. 2008

Braz J Med Biol Res

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Denervation of the colon is protective against the colon cancer; however, the mechanisms involved are unknown. We tested the hypothesis that the denervated colonic mucosa could be less responsive to the action of the chemical carcinogen dimethylhydrazine (DMH). Three groups of 32 male Wistar rats were treated as follows: group 1 (G1) had the colon denervated with 0.3 mL 1.5 mM benzyldimethyltetradecylammonium (benzalkonium chloride, BAC); G2 received a single ip injection of 125 mg/kg DMH; G3 was treated with BAC + the same dose and route of DMH. A control group (Sham, N = 32) did not receive any treatment. Each group was subdivided into four groups according to the sacrifice time (1, 2, 6, and 12 weeks after DMH). Crypt fission index, ß-catenin accumulated crypts, aberrant crypt foci, and cell proliferation were evaluated and analyzed by ANOVA and the Student t-test. G3 animals presented a small number of aberrant crypt foci and low crypt fission index compared to G2 animals after 2 and 12 weeks, respectively. From the second week on, the index of ß-catenin crypt in G3 animals increased slower than in G2 animals. From the 12th week on, G2 animals presented a significant increase in cell proliferation when compared to the other groups. Colonic denervation plays an anticarcinogenic role from early stages of colon cancer development. This finding can be of importance for the study of the role of the enteric nervous system in the carcinogenic process.

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“…The effect seems to involve the canonical Wnt signaling family because it was accompanied by nuclear accumulation of ␤-catenin ( Figure 4B). Some cases of cross talk between Wnt and insulin pathways have been reported (Fukumoto et al, 2001;Harwood, 2001), including on ␤-catenin activity (Papkoff, 1997;Playford et al, 2000;Desbois-Mouthon et al, 2001). The pool of GSK-3 targeted by Wnt is mostly nonphosphorylated by the insulin/PKB pathway (Ding et al, 2000).…”

Section: Gsk-3 Inhibition Is One Component In the Initiation Of Diffementioning

confidence: 99%

Insulin and Wnt1 Pathways Cooperate to Induce Reserve Cell Activation in Differentiation and Myotube Hypertrophy

Rochat

Fernandez

Vandromme

et al. 2004

MBoC

129

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During ex vivo myoblast differentiation, a pool of quiescent mononucleated myoblasts, reserve cells, arise alongside myotubes. Insulin/insulin-like growth factor (IGF) and PKB/Akt-dependent phosphorylation activates skeletal muscle differentiation and hypertrophy. We have investigated the role of glycogen synthase kinase 3 (GSK-3) inhibition by protein kinase B (PKB)/Akt and Wnt/␤-catenin pathways in reserve cell activation during myoblast differentiation and myotube hypertrophy. Inhibition of GSK-3 by LiCl or SB216763, restored insulin-dependent differentiation of C2ind myoblasts in low serum, and cooperated with insulin in serum-free medium to induce MyoD and myogenin expression in C2ind myoblasts, quiescent C2 or primary human reserve cells. We show that LiCl treatment induced nuclear accumulation of ␤-catenin in C2 myoblasts, thus mimicking activation of canonical Wnt signaling. Similarly to the effect of GSK-3 inhibitors with insulin, coculturing C2 reserve cells with Wnt1-expressing fibroblasts enhanced insulinstimulated induction of MyoD and myogenin in reserve cells. A similar cooperative effect of LiCl or Wnt1 with insulin was observed during late ex vivo differentiation and promoted increased size and fusion of myotubes. We show that this synergistic effect on myotube hypertrophy involved an increased fusion of reserve cells into preexisting myotubes. These data reveal insulin and Wnt/␤-catenin pathways cooperate in muscle cell differentiation through activation and recruitment of satellite cell-like reserve myoblasts. INTRODUCTIONSatellite cells are skeletal muscle adult stem cells that participate in postnatal muscle growth and regeneration. Although satellite cells are normally quiescent in adult muscle, they are responsible for muscle regeneration after injury and involved in work-or load-induced muscle fiber hypertrophy (Rosenblatt and Parry, 1992;Schultz and McCormick, 1994;De Angelis et al., 1999;Semsarian et al., 1999;Bodine et al., 2001).Ex vivo models such as myogenic cell lines were isolated from adult mouse muscle and as such are derived from adult satellite cells. At the proliferative stage, myoblasts (activated satellite cells) can be grown extensively in high serum-containing medium and express MyoD, a musclespecific transcription factor that regulates the differentiation process (Weintraub, 1993). When serum levels are lowered, myoblasts exit the cell cycle and spontaneously differentiate, giving rise to a heterogeneous population of cells. The first and major subpopulation is composed of myotubes, quiescent multinucleated cells expressing muscle-specific structural proteins. The remaining subset is composed of quiescent, mononucleated and undifferentiated cells termed reserve cells. Reserve cells retain the ability to be activated and proliferate after which they can be induced to differentiate, leading again to a new mixed population of myotubes and reserve cells. They also express at least two genes characteristic of skeletal muscle stem cells, namely, myf-5 and cd34 and from these c...

show abstract

Insulin-like growth factor 1 regulates the location, stability, and transcriptional activity of β-catenin

Cited by 256 publications

References 62 publications

Bcr-Abl induces autocrine IGF-1 signaling

Bcr-Abl induces autocrine IGF-1 signaling

Intrinsic denervation of the colon is associated with a decrease of some colonic preneoplastic markers in rats treated with a chemical carcinogen

Insulin and Wnt1 Pathways Cooperate to Induce Reserve Cell Activation in Differentiation and Myotube Hypertrophy

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