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Use of Recombinant DNA Technology for Engineering Mammalian Cells to Produce Proteins
Published in Anthony S. Lubiniecki, Large-Scale Mammalian Cell Culture Technology, 2018
The mechanism of amplification of a transfected CAD gene upon PALA selection has been extensively studied (67, 68). The integrated CAD sequence is first deleted and then undergoes replication as an extrachromosomal element. The extrachromosomal intermediate may increase in size by forming multiples of itself to eventually create double-minute chromosomes. The extrachromosomal sequence can eventually integrate to form a homogeneously staining chromosomal region.
Combination treatment with auranofin and nutlin-3a induces synergistic cytotoxicity in breast cancer cells
Published in Journal of Toxicology and Environmental Health, Part A, 2019
Dong-Jin Ye, Yeo-Jung Kwon, Hyoung-Seok Baek, Eunah Cho, Tae-Uk Kwon, Young-Jin Chun
p53, a protein encoded by TP53 gene is a well-known tumor-suppressing transcription factor. During intracellular stress conditions such as DNA damage, hypoxia, and oncogene activation, p53 expression is induced leading to diverse cellular responses including cell cycle arrest and apoptosis (Lee et al. 2016; Wang, Simpson, and Brown 2015). As p53-mediated intracellular signaling is a crucial factor in inhibiting tumor growth, several studies examined the possibility to develop efficient breast cancer therapies using p53 as a therapeutic target by implementing different approaches including wild-type p53 activation, mutant p53 reactivation, or p53-based vaccines (Hong et al. 2014). In many cases of breast cancer, p53-mediated mechanisms such as DNA damage-induced cell death and cell cycle regulation are often not activated due to overexpression of mouse double minute 2 homolog (MDM2) and MDMX. These protooncogenes function as E3 ubiquitin ligases and produce degradation of p53 (Wang and Yan 2011). Thus, one of the conventional therapeutic strategies for breast cancer treatment is the prevention of wild-type p53 from undergoing proteasomal degradation by MDM2 and efficiently retrieving the p53 pathway in the intra-tumoral environment (Turner et al. 2013).