Inhibitory effect of icariin on osteosarcoma cell proliferation via the Wnt/β-catenin signaling pathway

Abstract

Osteosarcoma, is a kind of malignant tumor derived from malignant interstitial cells. The pathogenesis of osteosarcoma remains unclear and despite use of chemotherapy drugs, resistance to these drugs affects the success of treatment. The present study was conducted to investigate the effects of icariin (ICA) on osteosarcoma cell proliferation and to investigate the role of the Wnt/β-catenin signaling pathway in the inhibition process of ICA on osteosarcoma cell proliferation. Different concentrations of ICA were selected to treat the osteosarcoma cell line 143B for 24 h, and then the onset concentration of ICA when it inhibited the growth of osteosarcoma cancer cell line 143B was detected via an MTT assay. The effect of ICA on the apoptosis of colon cancer cell line 143B under this concentration was detected using a flow cytometer. RNA in osteosarcoma cell line 143B was extracted, followed by reverse transcription. The expression levels of related and apoptotic proteins in the Wnt/β-catenin signaling pathway using ICA were detected by semi-quantitative PCR and western blot analysis, respectively. The expression quantities of vascular endothelial growth factor (VEGF) and MMP-9 were detected by ELISA. MTT assay showed that ICA inhibited the growth of 143B when its concentration was 5 µM (p<0.01). Flow cytometry showed that the number of apoptotic cells after ICA treatment was significantly higher than that in control group (p<0.01). RNA in osteosarcoma cell line 143B was extracted, followed by reverse transcription. Semi-quantitative PCR and western blot analysis revealed that the expression levels of p-GSK3β, β-catenin, c-Myc and cyclin D1 in cells after ICA treatment were significantly downregulated (p<0.01), while the expression level of caspase-3 was significantly increased (p<0.01). ELISA showed that the expression quantities of VEGF and MMP-9 were significantly decreased (p<0.01). Thus, ICA can significantly inhibit osteosarcoma cell proliferation and promote osteosarcoma cell apoptosis, which may be realized by affecting the expression of the Wnt/β-catenin signaling pathway and blocking the expression of related proteins.

Icariin suppresses cell cycle transition and cell migration in ovarian cancer cells

“…In contrast, p21 expression level was increased with ICA treatment. These results were consistent with previous research, indicating that ICA may inhibit tumor cell proliferation (36). The findings of the present study indicated that ICA may have increased G 1 cell cycle arrest and inhibited DNA synthesis in SKOV3 cells.…”

URG4 mediates cell proliferation and cell cycle in osteosarcoma via GSK3β/β-catenin/cyclin D1 signaling pathway

“…Additionally, Glycogen Synthase Kinase-3β (GSK-3β) is involved in cell cycle progression and proliferation of multiple tumors, including osteosarcoma [15]. The involvement of the β-catenin/cyclin D 1 pathway in cell proliferation and differentiation consider as a crucial signaling pathway [16].…”

Icariin affects cell cycle progression and proliferation of human retinal pigment epithelial cells via enhancing expression of H19

“…Recent efforts have been directed toward the biochemical inhibition of cellular proliferation in PVR, but the effect is not ideal. ICA is a pharmacologically active flavonoid that can suppress growth and promote apoptosis in a variety of malignant cells (Sun et al, 2016b;Ren, Zhu & Liu, 2018). Additionally, ICA prevents against mitogen-induced aberrant proliferation in other cell lines.…”

“…Recently, emerging studies have reported ICA regulates cell cycle progression and proliferation in various cell types. ICA exerted suppressive effects on medulloblastoma cells (Sun et al, 2016b), osteosarcoma cells (Ren, Zhu & Liu, 2018) and human aortic smooth muscle cells (HA-VSMCs) (Hu et al, 2016). Further, the induction of G0/G1 phase arrest was observed in cardiomyocyte and breast cancer cells after treatment with ICA (Zhu et al, 2005;Cheng et al, 2019).…”