The role of the IGF-1 Ec in myoskeletal system and osteosarcoma pathophysiology

Armakolas, Nikolaos; Armakolas, Athanasios; Antonopoulos, Athanasios; Dimakakos, Andreas; Stathaki, Martha; Koutsilieris, Michael

doi:10.1016/j.critrevonc.2016.11.004

Cited by 17 publications

(16 citation statements)

References 130 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, the precise mechanisms responsible for synchronizing bone and skeletal muscle mass remain unclear. Although basic studies have helped dissect the multiple influences of skeletal muscle on bone through cytokines such as myostatin, insulin-like growth factor 1 (IGF-1), fibroblast growth factor 2 (FGF-2), interleukin-6 (IL-6), IL-15, myostatin, osteoglycin (OGN), FAM5C, and osteoactivin [9][10][11][12][13][14], few osteokines involved in the feedback control of muscle by bone have been identified, with the exception of the osteocyte-specific Wnt family member 3a (Wnt3a), prostaglandin E2 (PGE2), osteoblast-derived IGF-1 and osteocalcin [15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

Osteocalcin Induces Proliferation via Positive Activation of the PI3K/Akt, P38 MAPK Pathways and Promotes Differentiation Through Activation of the GPRC6A-ERK1/2 Pathway in C2C12 Myoblast Cells

Liu

Gao

Wen

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Sarcopenia is characterized by an age-related decline in skeletal muscle plus low muscle strength and/or physical performance. Despite the clinical significance of sarcopenia, the molecular pathways underlying sarcopenia remain elusive. The recent demonstration that undercarboxylated osteocalcin (ucOC) favours muscle function related to insulin sensitivity and glucose metabolism raises the question of whether this hormone may also regulate muscle mass. The present study explored the promotive effects of ucOC in proliferation and differentiation processes of C2C12 myoblasts as well as the possible signalling pathways involved. Methods: The effects of exogenous ucOC on C2C12 myoblasts proliferation were assessed using CCK8 and immunohistological staining assays. C2C12 cells were pretreated with PI3K/Akt or P38 MAPK inhibitors to investigate the possible involvement of the PI3K/Akt and P38 MAPK pathways in proliferation. The levels of Akt, phosphorylatedAkt (p-Akt), P38, and phosphorylated-P38 (p-P38) were measured by Western Blotting. The effects of ucOC on myoblast differentiation were quantified by morphological analysis. A silencing experiment was conducted in which the expression of GPRC6A in C2C12 myoblasts was modified. The expression of GPRC6A, myosin heavy chain (MyHC) and the related ERK1/2 signalling pathway in C2C12 myoblasts were monitored by qRT-PCR and Western Blotting. Results: We showed that treatment with exogenous ucOC stimulated the priming

show abstract

Section: Introductionmentioning

confidence: 99%

Osteocalcin Induces Proliferation via Positive Activation of the PI3K/Akt, P38 MAPK Pathways and Promotes Differentiation Through Activation of the GPRC6A-ERK1/2 Pathway in C2C12 Myoblast Cells

Liu

Gao

Wen

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Bevacizumab, for instance, was the first anti-angiogenic agent approved for anti-angiogenic therapy (21), and has shown benefit in several solid tumors (22). Especially, VEGF inhibitors were widely studied to ameliorate the progression of osteosarcoma, such as muramyl tripeptide as an immunotherapy drug (23), IGF-1 as targeted therapy drug (24), Saracatinib (25) and desmopressin (26). In the present study, it was observed that SPOCD1 positively regulated the expression of VEGF-A at both the mRNA and protein levels.…”

Section: Discussionmentioning

confidence: 99%

SPOCD1 promotes cell proliferation and inhibits cell apoptosis in human osteosarcoma

Liang

Zhao

et al. 2017

Mol Med Report

View full text Add to dashboard Cite

Osteosarcoma is the most common type of malignant bone tumors that typically affects adolescents and children. The spen paralogue and orthologue C‑terminal domain containing 1 (SPOCD1) is a newly identified molecule that has been indicated to discriminate progressive from non‑progressive bladder cancers. However, the role of SPOCD1 in human solid tumors remains largely unknown. In the present study, SPOCD1 was upregulated in clinical osteosarcoma tissues compared with adjacent non‑cancerous tissues. Furthermore, SPOCD1 was upregulated in osteosarcoma cell lines and expression was particularly increased in highly invasive cells MG63 and SAOS2. Further investigation revealed that downregulation of SPOCD1 inhibited the MG63 and SAOS2 osteosarcoma cell colony formation and proliferation capacity. In addition, cell apoptosis was promoted by knockdown of SPOCD1 in MG63 and SAOS2 cells. These effects were confirmed by measuring the Ki67 and PCNA expression. In addition, SPOCD1 positively regulated the expression of vascular endothelial growth factor A (VEGF‑A). Knockdown of VEGF‑A blunted SPOCD1 downregulation‑mediated inhibition of cell proliferation and induction of cell apoptosis. These results suggested that SPOCD1 may act as a pro‑oncogenic factor in osteosarcoma. Inhibition of VEGF may aid in treating osteosarcoma in clinic.

show abstract

“…Dünya Sağlık Örgütü'nün yaş sınıflamasına göre çoklu primer tümörler ileri yaş grubunda (>65 yaş) daha sık görülmektedir. Bu da yaşlanmanın kanser gelişiminde bir risk faktörü olduğunu düşündürmektedir [11][12] . Aynı anda iki primer senkron malignite nadir görülmekle birlikte bir literatürde birden fazla primer malignite varlığı önceye nazaran artık daha fazla görüldüğü, ikinci primer kanser insidansının indeks primer kansere bağlı olarak %1 ila %16 arasında değişmekte olduğu bildirilmiştir [17] .…”

Section: Discussionunclassified

Synchronous Pancreatic Ductal Adenocarcinoma and Thyroid Medullary Carcinoma

Göret¹

2017

Haydarpasa Numune Med J

View full text Add to dashboard Cite

M ultipl kanserler, metakron ve senkron tümörler olarak sınıflandırılmaktadır. Tümör aynı ya da çok kısa zaman aralığı içinde saptanırsa senkron, ikinci tümör birinciyi takiben 12 ay ya da daha uzun bir süre sonra saptanırsa metakron tümör olarak tanımlanmaktadır [1,2]. Multipl primer tümörlerin literatürde tüm karsinomaların %0.7-11.7'si oranında olduğu bildirilmektedir [4,6]. Oluşum mekanizmaları tam olarak bilinmemektedir. Karsinogeneze ilişkin bazı teo-riler ortaya atılmıştır [7,10]. Genetik fonksiyon bozukluğu, gen mutasyonu, genetik instabilite gibi patolojilerde çoklu kanser gelişiminin tetiklenebileceği öne sürülmektedir. Ayrıca kemoterapi ve radyoterapi uygulamaları ve yaşam süresinin uzaması ikinci malignite gelişimini artırmaktadır [7,10,11]. Bu olgu sunumunda ilk olarak pankreasında kitle sonucu "pankreatik duktal adenokarsinom" olan olguda, 10 ay sonra tiroidinde ki nodül "medüller karsinom" olarak rapor Günümüzde ilerleyen tedavi yöntemleriyle kanserli hastaların sağ kalım süresi uzamıştır. Bu nedenle ikincil primer tümör görülme sıklığında artış gözlenmektedir. Hastanemize başvuran 52 yaşındaki erkek hastada senkron pankreas duktal adenokarsinomu ve tiroid medüller karsinom tespit edildi. Bu iki tümör birlikteliği daha önce bildirilmediğinden literatürde paylaşmayı amaçladık.

show abstract

The role of the IGF-1 Ec in myoskeletal system and osteosarcoma pathophysiology

Cited by 17 publications

References 130 publications

Osteocalcin Induces Proliferation via Positive Activation of the PI3K/Akt, P38 MAPK Pathways and Promotes Differentiation Through Activation of the GPRC6A-ERK1/2 Pathway in C2C12 Myoblast Cells

Osteocalcin Induces Proliferation via Positive Activation of the PI3K/Akt, P38 MAPK Pathways and Promotes Differentiation Through Activation of the GPRC6A-ERK1/2 Pathway in C2C12 Myoblast Cells

SPOCD1 promotes cell proliferation and inhibits cell apoptosis in human osteosarcoma

Synchronous Pancreatic Ductal Adenocarcinoma and Thyroid Medullary Carcinoma

Contact Info

Product

Resources

About