SOST silencing promotes proliferation and invasion and reduces apoptosis of retinoblastoma cells by activating Wnt/β-catenin signaling pathway

Abstract

This study aimed to investigate the effects of SOST and the Wnt/β-catenin signaling pathway on the proliferation, migration, invasion, and apoptosis of human retinoblastoma cells. Fifty-five retinoblastoma and 21 normal retinal tissue samples were collected as the case group and control group, respectively. HXO-RB44 and SO-RB50 cells were selected and assigned into blank, negative control (NC), siRNA 1, siRNA 2, siRNA 3, IWR-1-endo 1, IWR-1-endo 2 and IWR-1-endo 3 groups. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to detect the expression of SOST, Wnt-1, and β-catenin in the collected tissue samples. MTT assay, flow cytometry, transwell assay and the starch test were employed to determine the cell proliferation, cell cycle, apoptosis, invasion and migration after transfection. The qRT-PCR and western blotting were also used to detect the mRNA and protein expressions of SOST, Wnt-1, β-catenin, C-myc, Cyclin D1, MMP-2 and MMP-9. The tumor formation in nude mice was conducted to evaluate the effects of SOST on the growth of a transplanted tumor. Compared with normal retinal tissues, the retinoblastoma tissues exhibited a downregulation of SOST but an upregulation of Wnt-1 and β-catenin. The proliferation, invasion and migration of HXO-RB44 and SO-RB50 cells in the SOST-siRNA group were significantly higher than the cells in the blank and NC groups. The expressions of Wnt-1, β-catenin, C-myc, Cyclin D1, MMP-2 and MMP-9 in the three SOST-siRNA groups were elevated, but the SOST decreased when compared with the blank and NC groups. SOST silencing promoted the growth of transplanted tumors in nude mice. These findings indicate that SOST silencing promotes the proliferation, invasion and migration, and decreases the apoptosis of human retinoblastoma cells by activating the Wnt/β-catenin signaling pathway.

LINC01128 regulates the development of osteosarcoma by sponging miR‐299‐3p to mediate MMP2 expression and activating Wnt/β‐catenin signalling pathway

“…A previous study demonstrated that OS progression is associated with the transcriptional activity of activated β‐catenin 23 . Besides, some studies have also shown that MMP2 is closely associated with the Wnt/β‐catenin signalling pathway 24‐26 . This study validates that LINC01128 affects MMP2 mRNA stability through competitive binding with miR‐299‐3p.…”

“…23 Besides, some studies have also shown that MMP2 is closely associated with the Wnt/β-catenin signalling pathway. [24][25][26] This study…”

Cell cycle defects underlie childhood-onset cardiomyopathy associated with Noonan syndrome

“…It is therefore plausible that an aberrant increase of FGF10 expression is driving left ventricular cardiomyocyte proliferation in NS-CM. Similarly, the upregulation of EREG and downregulation of FOSB and SOST that we observed in NS-CM have previously been associated with increased cell proliferation in a number of physiological and cancerous processes ( Cao et al., 2013 ; Kyotani et al., 2013 ; Morato et al., 2021 ; Nishioka et al., 2020 ; White et al., 2010 ; Wu et al., 2017 ; Xu et al., 2017 ; Zhang et al., 2020 ; Zou et al., 2017 ). As an upstream component of the Ras-MAPK pathway, the EGFR ligand EREG is a particularly interesting candidate for further studies of the mechanisms of NS-CM.…”

Silencing myelin protein zero-like 1 expression suppresses cell proliferation and invasiveness of human glioma cells by inhibiting multiple cancer-associated signal pathways

“…MMP-2 is a member of the metalloproteinase family, which degrades various components of the extracellular matrix, changes the microenvironment of tumors, and facilitates tumor cell migration [32,33]. The migration of glioma cells is special, and they actively migrate and this is achieved in two ways: through the perivascular space and the brain parenchyma.…”