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.
NEO217 cells and available osteosarcoma cell lines such as MG-63 and MNNG/HOS were all CD29<sup>+</sup>CD59<sup>+</sup> phenotype as detected by flow cytometry.
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.
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.
Soluble chromium (VI) compounds either alone or in combination with 3-methylcholanthrene (MC) were used to transform non-tumorigenic osteoblast-like human osteosarcoma cells (HOS TE85).
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.
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.
The HOSosteosarcoma cell line (also known as TE-85), which express the normal-sized 2.5 kb BLK-ALP mRNA only, exhibited ALP activity with kinetic properties of both the BLK and PL-/PL-like isoenzymes.
In this study, we report a systematic investigation of the cytotoxicity and in vivo biodistribution of G/SWCNT hybrids on osteosarcoma cells (HOS and U2OS).
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.
Prostate-specific antigen (PSA)-mediated proliferation, androgenic regulation and inhibitory effects of LY312340 in HOS-TE85 (TE85) human osteosarcoma cells.
The antitumor activity of [bpyH][VO(nta)(H<sub>2</sub>O)]H<sub>2</sub>O and its phenanthroline analogue, [phenH][VO(nta)(H<sub>2</sub>O)](H<sub>2</sub>O)<sub>0.5</sub>, towards human osteosarcoma cell lines (MG-63 and HOS) has been assessed (the LDH and BrdU tests) and referred to cis-Pt(NH<sub>3</sub>)<sub>2</sub>Cl<sub>2</sub> (used as a positive control).
Although the human osteosarcoma cell lines HOS and MG63 have a wild-type RB gene, SaOS-2 and OSrb (established from retinoblastoma patient) have no active RB gene.
We found that Oridonin at sub-toxic concentrations synergistically enhanced Nutlin-3-mediated cell viability inhibition in wild-type p53 U2OS and SJSA-1, but not in p53-mutant MNNG/HOS and in null-p53 Saos-2 osteosarcoma cell lines.