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.
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.
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.
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.
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.
Very low levels of adenovirus cellular receptor coxsackievirus/adenovirus receptor (CAR) (Ad5 receptor) expression were observed in MNNG-HOS and MG-63 cells, whereas high levels of CAR expression were seen in the other osteosarcoma cell lines.
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.
To investigate the role of YAP1 in osteosarcoma tumorigenesis, the expression of YAP1 in the osteosarcoma cell lines (MG-63 and HOS) was knocked down by small hairpin RNA (shRNA), and the cell proliferation and colony formation assay showed that knockdown of YAP1 significantly suppressed the cell proliferation and colony formation of osteosarcoma cells.
To examine the antitumor effects of gallic acid (GA) on osteosarcoma, two human osteosarcoma cell lines U-2OS and MNNG/HOS were treated by GA and subjected to cell proliferation and apoptosis assays.
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.
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.
Thus, in addition to the recent discovery of estradiol receptors and estrogenic regulation of HOS TE85 cells, it is now evident that these osteoblast-like osteosarcoma cells also express high affinity androgen binding sites and can respond biologically to androgens.
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.
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.
The roles of miR-142-3p in osteosarcoma development were studied using cultured HOS, MG63 and Saos-2 cells and tumor xenograft analyses in nude mice; their target genes were also investigated.
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 mRNA and protein levels of ANXA3 in the osteosarcoma cell lines HOS and U2OS were significantly increased compared with osteoblasts, particularly in HOS 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.
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).