Knockdown of galectin-1 suppresses the growth and invasion of osteosarcoma cells through inhibition of the MAPK/ERK pathway

Miao, Jinhao; Wang, Shuqiang; Zhang, Minghui; Yu, Feng‑Bin; Zhang, Lei; Yu, Zhongxiang; Kuang, Yong

doi:10.3892/or.2014.3358

Cited by 31 publications

(21 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…5A, downregulation of galectin-3 markedly inhibited the activity of MEK/ERK signaling (P<0.01), suggesting that the MEK/ERK signaling pathway may act as a downstream effector of the malignant properties of MG63 cells. As the MEK/ERK signaling pathway has been demonstrated to be involved in the regulation of OS-cell invasion (11,12), the present study used curcumin, an agonist of MEK, to upregulate the activity of the MEK/ERK signaling pathway. As shown in Fig.…”

Section: Knockdown Of Galectin-3 Suppresses Migration and Invasion Ofmentioning

confidence: 99%

Small interfering RNA-induced silencing of galectin-3 inhibits the malignant phenotypes of osteosarcoma in vitro

Lei

et al. 2015

Molecular Medicine Reports

View full text Add to dashboard Cite

Osteosarcoma (OS) is the most common malignant tumor of bone. It has recently been demonstrated that galectin-3, a multifunctional β-galactoside-binding, is significantly upregulated in OS tissues, and is correlated with its progression and metastasis. However, the detailed role of galectin‑3 in the regulation of cellular biological processes in OS cells has remained to be elucidated. The present study reported that the mRNA and protein levels of galectin‑3 were significantly increased in OS tissues compared to those in their matched normal adjacent tissues. Furthermore, galectin‑3 was upregulated in three OS cell lines, Saos‑2, MG63 and U2OS, when compared with that in the human osteoblast cell line hFOB1.19. Knockdown of galectin‑3 by galectin‑3‑specific small interfering RNA markedly inhibited OS‑cell proliferation and induced cell apoptosis. Furthermore, silencing of galectin‑3 expression significantly inhibited OS cell migration and invasion, accompanied with a marked decrease in the protein expression of matrix metalloproteinase 2 and ‑9. Mechanistic investigation suggested that the mitogen‑activated protein kinase kinase/extracellular signal‑regulated protein kinase signaling pathway may be involved in the galectin‑3‑mediated OS cell invasion. In conclusion, the present study was the first to report that silencing of galectin‑3 inhibited the malignant phenotypes of osteosarcoma in vitro. Therefore, galectin-3 may serve as a potential therapeutic target for OS.

show abstract

Section: Knockdown Of Galectin-3 Suppresses Migration and Invasion Ofmentioning

confidence: 99%

Small interfering RNA-induced silencing of galectin-3 inhibits the malignant phenotypes of osteosarcoma in vitro

Lei

et al. 2015

Molecular Medicine Reports

View full text Add to dashboard Cite

show abstract

“…Of note, we identified 10 hub IRGs, namely CXCR3, CXCR4, CCR5, CCL5, CXCL10, CXCL12, CXCL16, OPRL1, S1PR1, and GAL. Among them, CXCR3 28 , CXCR4 29 , CCR5 30 , CCL5 31 , CXCL16 32 , CXCL10 33 , CXCL12 34 and GAL 35 have been widely studied in OS, and are involved in the occurrence, metastasis, and angiogenesis of OS. OPRL1 encodes proteins that are endogenous opioid-related neuropeptides and nociceptin/orphanin receptors, which plays a key role in pain perception and nociception 36 , 37 .…”

Section: Discussionmentioning

confidence: 99%

Development of a novel immune-related genes prognostic signature for osteosarcoma

Deng

Zhang

et al. 2020

Sci Rep

View full text Add to dashboard Cite

Immune-related genes (IRGs) are responsible for osteosarcoma (OS) initiation and development. We aimed to develop an optimal IRGs-based signature to assess of OS prognosis. Sample gene expression profiles and clinical information were downloaded from the Therapeutically Applicable Research to Generate Effective Treatments (TARGET) and Genotype-Tissue Expression (GTEx) databases. IRGs were obtained from the ImmPort database. R software was used to screen differentially expressed IRGs (DEIRGs) and functional correlation analysis. DEIRGs were analyzed by univariate Cox regression and iterative LASSO Cox regression analysis to develop an optimal prognostic signature, and the signature was further verified by independent cohort (GSE39055) and clinical correlation analysis. The analyses yielded 604 DEIRGs and 10 hub IRGs. A prognostic signature consisting of 13 IRGs was constructed, which strikingly correlated with OS overall survival and distant metastasis (p < 0.05, p < 0.01), and clinical subgroup showed that the signature’s prognostic ability was independent of clinicopathological factors. Univariate and multivariate Cox regression analyses also supported its prognostic value. In conclusion, we developed an IRGs signature that is a prognostic indicator in OS patients, and the signature might serve as potential prognostic indicator to identify outcome of OS and facilitate personalized management of the high-risk patients.

show abstract

“…For example, Barrionuevo and colleagues showed that soluble galectin-1 stimulated ERK-1/2 phosphorylation in human monocytes, and that inhibiting the upstream kinase MEK could reverse the effects of galectin-1 on macrophage major histocompatibility complex II and fragment crystallizable gamma receptor I expression 10 . Galectin-1 stimulation has further been shown to activate ERK in airway epithelium 44 and correlates with ERK activity in allergic conjunctivitis 45 , osteosarcoma growth 46 , and lung cancer progression 47 .…”

Section: Discussionmentioning

confidence: 99%

“…in allergic conjunctivitis 45 , osteosarcoma growth, 46 and lung cancer progression. 47 This ERK-mediated signaling is distinct from the myeloid differentiation primary response gene 88-dependent signaling we have noted on PDO fibers.…”

Section: Discussionmentioning

confidence: 99%

Galectin‐1 promotes an M2 macrophage response to polydioxanone scaffolds

Abebayehu

Spence

Boyan

et al. 2017

J Biomedical Materials Res

View full text Add to dashboard Cite

Regulating soft tissue repair to prevent fibrosis and promote regeneration is central to creating a microenvironment conducive to soft tissue development. Macrophages play an important role in this process. Their response can be modulated using biomaterials, altering cytokine and growth factor secretion to promote regeneration. Electrospun polydioxanone (PDO) fiber scaffolds promoted an M2 phenotype when macrophages were cultured on large diameter, highly porous scaffolds, but an M1 phenotype on smaller diameter fibers. Here we investigated whether incorporation of galectin-1, an immunosuppressive protein that enhances muscle regeneration, could promote the M2 response. Galectin-1 was incorporated into large and small fiber PDO scaffolds during electrospinning. Galectin-1 incorporation increased arginase-1 and reduced iNOS and IL-6 production in mouse bone-marrow derived macrophages compared to PDO alone for both scaffold types. Inhibition of ERK mitogen activated protein kinase did not alter galectin-1 effects on arginase-1 and iNOS expression, but reversed IL-6 suppression, indicating that IL-6 is mediated by a different mechanism. Our results suggest that galectin-1 can be used to modulate macrophage commitment to a pro-regenerative M2 phenotype, which may positively impact tissue regeneration when using small diameter PDO scaffolds.

show abstract

Knockdown of galectin-1 suppresses the growth and invasion of osteosarcoma cells through inhibition of the MAPK/ERK pathway

Cited by 31 publications

References 28 publications

Small interfering RNA-induced silencing of galectin-3 inhibits the malignant phenotypes of osteosarcoma in vitro

Small interfering RNA-induced silencing of galectin-3 inhibits the malignant phenotypes of osteosarcoma in vitro

Development of a novel immune-related genes prognostic signature for osteosarcoma

Galectin‐1 promotes an M2 macrophage response to polydioxanone scaffolds

Contact Info

Product

Resources

About