Coordinated effects of insulin-like growth factor I on inhibitory pathways of cell cycle progression in cultured cardiac muscle cells.

Atherosclerosis is a major cause of cardiovascular disease, in which vascular smooth muscle cells (VSMCs) proliferation and migration play a vital role. Circular RNAs (circRNAs) have been reported to be correlated with the VSMCs function. Therefore, this study is designed to explore the role and mechanism of circRNA lipase maturation factor 1 (circLMF1) in Human aortic VSMCs (HASMCs). The microarray was used for detecting the expression of circLMF1 in proliferative and quiescent HASMCs. Levels of circLMF1, microRNA-125a-3p (miR-125a-3p), vascular endothelial growth factor A (VEGFA), and fibroblast growth factor 1 (FGF1) were determined by real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability, cell cycle progression, and migration were assessed by Cell Counting Kit-8 (CCK-8), flow cytometry, wound healing, and transwell assays, respectively. Western blot assay determined proliferating cell nuclear antigen (PCNA), Cyclin D1, matrix metalloproteinase (MMP2), osteopontin (OPN), VEGFA, and FGF1 protein levels. The possible interactions between miR-125a-3p and circLMF1, and miR-125a-3p and VEGFA or FGF1 were predicted by circbank or targetscan, and then verified by a dual-luciferase reporter, RNA Immunoprecipitation (RIP), RNA pull-down assays. CircLMF1, VEGFA, and FGF1 were increased, and miR-125a-3p was decreased in platelet-derived growth factor-BB (PDGF-BB)-inducted HASMCs. Functionally, circLMF1 knockdown hindered cell viability, cell cycle progression, and migration in PDGF-BB-treated HASMCs. Mechanically, circLMF1 could regulate VEGFA or FGF1 expression through sponging miR-125a-3p. Our findings revealed that circLMF1 deficiency could inhibit cell viability, cell cycle progression, and migration of PDGF-BB stimulated atherosclerosis model partly through the miR-125a-3p/VEGFA or FGF1 axis, suggesting that targeting circLMF1 can be a feasible therapeutic strategy for atherosclerosis.

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Lycopene Interferes With Cell Cycle Progression and Insulin-Like Growth Factor I Signaling in Mammary Cancer Cells

Nutrition and Cancer ◽

10.1207/s15327914nc3601_14 ◽

2000 ◽

Vol 36 (1) ◽

pp. 101-111 ◽

Cited By ~ 224

Author(s):

Michael Karas ◽

Hadar Amir ◽

Daniel Fishman ◽

Michael Danilenko ◽

Shraga Segal ◽

...

Keyword(s):

Cell Cycle ◽

Growth Factor ◽

Cancer Cells ◽

Mammary Cancer ◽

Cell Cycle Progression ◽

Insulin Like Growth Factor ◽

Cycle Progression ◽

Factor I ◽

Growth Factor I ◽

Mammary Cancer Cells

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Activin A inhibits cell-cycle progression induced by insulin-like growth factor-I in Balb/c 3T3 cells

Journal of Endocrinology ◽

10.1677/joe.0.1370099 ◽

1993 ◽

Vol 137 (1) ◽

pp. 99-105 ◽

Cited By ~ 4

Author(s):

I. Kojima ◽

H. Mogami ◽

N. Kawamura ◽

H. Shibata

Keyword(s):

Cell Cycle ◽

Growth Factor ◽

Cell Cycle Progression ◽

Activin A ◽

3T3 Cells ◽

Cycle Progression ◽

Factor I ◽

Competent Cells ◽

Igf I ◽

Mediated Reduction

ABSTRACT The present study was carried out to examine the effect of activin A on cell-cycle progression induced by insulin-like growth factor-I (IGF-I) in Balb/c 3T3 cells. When activin A was added together with IGF-I to competent cells primed with epidermal growth factor (primed competent cells), both [3H]thymidine incorporation and nuclear labelling induced by IGF-I were inhibited. The inhibition was concentration-dependent and the maximum inhibition was obtained with 1 nmol activin A/l. To ascertain the time in which activin A exerted its inhibitory action, we divided 12 h, the time required for primed competent cells to progress towards the S phase, into four periods and activin A was added during each of the four periods. It was effective when added during either the second (3 to 6 h) or the third period (6 to 9 h) but it did not affect cell-cycle progression when added during the first (0 to 3 h) or the last period (9 to 12 h). We then examined whether activin A affected intracellular events elicited by IGF-I. It did not affect either autophosphorylation of the IGF-I receptor or calcium entry induced by IGF-I. Likewise, it did not cause any change in the radioactivity of 1,2-diacylglycerol (DAG) in cells prelabelled with [3H]myristate while the increase in the mass of DAG induced by IGF-I was markedly reduced by activin A. The dose-response relationship for the activin A-mediated reduction of DAG mass correlated well with that for the activin A-mediated reduction of DNA synthesis. Activin A was effective in reducing DAG mass even when added 3 h after the addition of IGF-I. These results indicate that activin A attenuates cell-cycle progression in the middle of the G1 phase. The results also raise the possibility that reduction of DAG mass may account for the inhibitory effect of activin A on cell-cycle progression. Journal of Endocrinology (1993) 137, 99–105

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Insulin-like growth factor-I prevents hypoxia-inducible factor-1 alpha-dependent G1/S arrest by activating cyclin E/cyclin-dependent kinase2 via the phoshatidylinositol-3 kinase/AKT/forkhead box O1/Cdkn1b pathway in porcine granulosa cells†

Biology of Reproduction ◽

10.1093/biolre/ioz162 ◽

2019 ◽

Cited By ~ 1

Author(s):

Chengyu Li ◽

Zhaojun Liu ◽

Jiaqi Zhou ◽

Xueqin Meng ◽

Shuo Liu ◽

...

Keyword(s):

Cell Cycle ◽

Growth Factor ◽

Granulosa Cells ◽

Cell Cycle Progression ◽

Hypoxia Inducible Factor ◽

Inhibitory Effects ◽

Cycle Progression ◽

Hypoxia Inducible Factor 1 ◽

Factor I ◽

Igf I

Abstract As the follicle develops, the thickening of the granulosa compartment leads to progressively deficient supply of oxygen in granulosa cells (GCs) due to the growing distances from the follicular vessels. These conditions are believed to cause hypoxia in GCs during folliculogenesis. Upon hypoxic conditions, several types of mammalian cells have been reported to undergo cell cycle arrest. However, it remains unclear whether hypoxia exerts any impact on cell cycle progression of GCs. On the other hand, although the GCs may live in a hypoxic environment, their mitotic capability appears to be unaffected in growing follicles. It thus raises the question whether there are certain intraovarian factors that might overcome the inhibitory effects of hypoxia. The present study provides the first evidence suggesting that cobalt chloride (CoCl2)-mimicked hypoxia prevented G1-to-S cell cycle progression in porcine GCs. In addition, we demonstrated that the inhibitory effects of CoCl2 on GCs cell cycle are mediated through hypoxia-inducible factor-1 alpha/FOXO1/Cdkn1b pathway. Moreover, we identified insulin-like growth factor-I (IGF-I) as an intrafollicular factor required for cell cycle recovery by binding to IGF-I receptor in GCs suffering CoCl2 stimulation. Further investigations confirmed a role of IGF-I in preserving G1/S progression of CoCl2-treated GCs via activating the cyclin E/cyclin-dependent kinase2 complex through the phoshatidylinositol-3 kinase/protein kinase B (AKT)/FOXO1/Cdkn1b axis. Although the present findings were based on a hypoxia mimicking model by using CoCl2, our study might shed new light on the regulatory mechanism of GCs cell cycle upon hypoxic stimulation.

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