Polyethylene glycols are synthetic polymers composed of repeating oxyethylene subunits, which have been known for non-toxic, non-immunogenic, non-antigenic, good solubility in water and therefore approved for pharmaceutical applications. Recently, attachment or amalgamation of polyethylene glycols to therapeutic small molecules, peptides, proteins, or nanoparticles has become a mature technology for the sake of improving their pharmacokinetic and pharmacological profiles, also referred to as PEGylation. By comparison, there are only a few PEGylated pharmaceuticals have been registered for further clinical trials and even less was approved for marketing. High failure rate of PEGylated pharmaceuticals in pre-clinical and clinical trials could be majorly attributed to their unclear pharmacokinetic behaviors. Therefore, the in vivo fate of the PEGylated pharmaceuticals for the various routes of administration needs to be thoroughly investigated An accurate in vivo pharmacological study thereof highly depends on the precise detection of polyethylene glycols as well as their fragments in biological matrixes. The goal of this review is to highlight the analytical methods that were developed and applied to evaluate the polyethylene glycols in pharmaceutical ingredients and excipients, which bring us closer to bridging
Among the newly diagnosed cancers in women, breast cancer metastasis is a key factor contributing to the poor prognosis. BMSCs are critical components for the malignant microenvironment. Studies have shown that the interaction between tumor cells and BMSCs support breast cancer progression.
However, BMSCs’ effect on breast cancer cells is not yet clear. BMSCs and breast cancer cell MCF-7 were co-cultured to analyze tumor cell proliferation and apoptosis along with analysis of E-cadherin and Vimentin expression by real-time PCR, interleukin-6 and matrix protease-2 and PTEN12
expression. Co-culture of BMSCs promoted breast cancer cell proliferation, decreased apoptosis-related Caspase 3 activity and downregulated the expression of EMT related factors, upregulated IL-6 secretion and MMP-2, and downregulated PTEN12 expression (P < 0.05). In conclusion,
BMSCs can promote breast cancer cell proliferation and survival and affect breast cancer transformation possibly through inhibiting the expression of PTEN12.
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