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.
Western analysis suggested that saurolactam treatment resulted in a reduction of Akt/PKB, phospho-Ser473-Akt, c-Myc, and S-phase kinase-associated protein 2 (Skp2) in MG-63 and HOSosteosarcoma cells.
Knockdown of WWP1 using small interfering RNA further showed that deficiency of WWP1 blocked cell growth and cell invasion, and caused G1-phase arrest and cell apoptosis in osteosarcoma cells (MG63 and HOS).
We used isobaric tags for relative and absolute quantitation (iTRAQ) and nanoscale liquid chromatography-mass spectrometry (NanoLC-MS/MS) to identify differentially expressed proteins in MNNG/HOS and U2OS osteosarcoma cell lines transfected with miR-542-5p; in both cell lines, seven proteins were downregulated, and nine were upregulated.
Thus, the authors collected OS tissues (n = 15) and corresponding paracancerous tissues (n = 15) and found that the expression of miR-548c-3p was significantly downregulated in OS tissues and cell lines 143B, SaoS2, and HOS when compared to the corresponding paracancerous tissues and human osteoblast cell line hFOB (OB3), respectively.
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).
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.
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 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).
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.
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 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.
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.
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.
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.
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.