Abstract
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.
Highlights
MiR-21-5p has been reported to be one of the most abundant in exosomes derived from Growth hormone (GH)-secreting pituitary adenoma and downregulated the Programmed cell death 4/Activator protein 1 (PDCD4/AP-1) pathway by targeting PDCD4 and SMAD Family Member 7 (Smad7) [67] with subsequent distant effects that have been shown in vitro, osteoblast proliferation, differentiation and mineralization [67]
This review highlights the role for miRNAs and long non-coding RNAs (lncRNAs) in regulating genes related with Growth hormone (GH) and insulin-like growth factor (IGF) signaling in the context of cancer
We focused on the role of miRNAs and lncRNAs in pituitary adenomas, osteosarcoma and colorectal cancer (CRC), which are known to be tightly related with GH and the IGF system
Summary
MiR-21-5p has been reported to be one of the most abundant in exosomes derived from GH-secreting pituitary adenoma and downregulated the Programmed cell death 4/Activator protein 1 (PDCD4/AP-1) pathway by targeting PDCD4 and SMAD Family Member 7 (Smad7) [67] with subsequent distant effects that have been shown in vitro, osteoblast proliferation, differentiation and mineralization [67]. MiR-16 overexpression reduced cell proliferation in vitro and tumor growth in mice by targeting directly the IGF1R with subsequent inhibition of the Raf1- Mitogen-Activated Protein Kinase Kinase 1/2 (MEK1/2)-ERK1/2 pathway [77].
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