Herein, APTR expression was demonstrated to be significantly upregulated in OS tumor tissues and four OS cell lines (including MG63, 143B, Saos-2, and HOS) compared with the adjacent tissues and human osteoblast cell line hFOB1.19, respectively.
The mRNA and protein levels of ANXA3 in the osteosarcoma cell lines HOS and U2OS were significantly increased compared with osteoblasts, particularly in HOS cells.
To confirm the influence of per2 gene on MNNG/HOS human osteosarcoma cells, small interfering (si)RNA against per2 or plasmids containing per2 were transfected into MNNG/HOS cells, and the proliferation, apoptosis and migration were observed.
Using the multiple methods to detect the activity of PF on HOS and Saos‑2 human osteosarcoma cell lines, including an MTS assay, flow cytometry, transmission electron microscopy and western blotting, it was demonstrated that PF induces inhibition of proliferation, G2/M phase cell cycle arrest and apoptosis in the osteosarcoma cell lines in vitro, and activation of cleaved‑caspase‑3 and cleaved‑poly (ADPribose) polymerase in a dose‑dependent manner.
Overexpression of miR‑186 inhibited cell proliferation, arrested the cell cycle progression and suppressed the cell invasion of the HOS and U2 OS cell lines.
This peptide specifically was found to bind to the CD105‑positive osteosarcoma MNNG/HOS cell line and the osteosarcoma cells in the histological sections derived from an MNNG/HOS xenograft model and osteosarcoma patients in vitro.
We then utilized the CRISPR-Cas9 system to specifically silence CD44 in highly metastatic human osteosarcoma cells (MNNG/HOS and 143B) and further determined the functional effects of CD44 knockout in these cells.
The elevated level of NEAT1 was confirmed in OS cell lines including MG63 and HOS <i>in vitro</i> Knockdown of NEAT1 by two siRNAs induced impaired cell vitalities, promoted the apoptosis, and G<sub>0</sub>/G<sub>1</sub> arrest in two cell lines, which was associated with inhibited anti-apoptosis signals BCL-2 pathway and cell cycle-related cyclin D1 (CCND1) signals.
Interestingly, MTT assays in MG-63 and MNNG/HOSosteosarcoma cells exhibited that half-maximal inhibitory concentration (IC<sub>50</sub>) value of RGD-DOX-PM was much lower than its non-targeted counterpart (DOX-PM), implying RGD decorated nanoparticles had enhanced cell targeting ability and led to more effective anti-tumor effect.
As a potential strategy, we found that co-treatment with metformin significantly decreased the half maximal inhibitory concentration (IC50) of cisplatin to HOSOS stem cells by downregulating the expression of PKM2.