Adenoviral mediated overexpression and knockdown of IGFBP5 in the MG63 and MG63.2 cell lines, as well as other OS lines (143B and MNNG/HOS) that are independent of our MG63 lines, were employed to examine the role of IGFBP5.
Cell lines derived from pediatric patients with OS (HOS, MG63, 143B, KHOS-312H, U2-OS and SJSA1) were infected with MV expressing green fluorescent protein (MV-GFP) and MV-expressing sodium iodide symporter (MV-NIS) strains.
We also investigated whether there was an association between TP53 mutation and centrosome aberrations in the generation of chromosomal aneuploidy in OS in four OS cell lines (HOS, SAOS2, U2OS, and MG63) and in a subset of seven tumors.
The 143B-GFP cell line with high metastatic potential and the MNNG/HOS-RFP cell line with low metastatic potential, both derived from the TE85 human osteosarcoma cell line, were either co-transplanted or transplanted alone in the tibia in nude mice.
In conclusion, the HOS 58 osteosarcoma cell line represents a differentiated cell line with highly expressed and physiologically regulated AP expression during further differentiation in culture.
The results indicate that our DXR-resistant variants of MNNG/HOS and MG63 reveal a classical MDR phenotype and can offer a model with which to investigate the mechanisms of multidrug resistance in osteosarcoma.
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.
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.
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.
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.
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.
Prostate-specific antigen (PSA)-mediated proliferation, androgenic regulation and inhibitory effects of LY312340 in HOS-TE85 (TE85) human osteosarcoma cells.
Furthermore, the responses of human osteosarcoma (HOS MG63) cells cultured onto the scaffolds demonstrate that the viability of cells were considerably high for CNF-incorporated PCL/M-HAP than for PCL/M-HAP.
MPPa-PDT-resistant cells are isolated from the human osteosarcoma MG63 and HOS cell lines and two resistant populations were finally acquired, including MG63/PDT and HOS/PDT.
This resulted in inhibition of proliferation of osteosarcoma cell lines U-2 OS and HOS, but not of 143B, which harbors a KRAS oncogenic transformation.