Department of Biomedical Engineering, Stony Brook University, Stony Brook, NY 11794.
The Louis and Beatrice Laufer Center for Physical and Quantitative Biology, Stony Brook University, Stony Brook, NY 11794.
Proc Natl Acad Sci U S A. 2023 Dec 5;120(49):e2303114120. doi: 10.1073/pnas.2303114120. Epub 2023 Nov 29.
Drug resistance continues to impede the success of cancer treatments, creating a need for experimental model systems that are broad, yet simple, to allow the identification of mechanisms and novel countermeasures applicable to many cancer types. To address these needs, we investigated a set of engineered mammalian cell lines with synthetic gene circuits integrated into their genome that evolved resistance to Puromycin. We identified DNA amplification as the mechanism underlying drug resistance in 4 out of 6 replicate populations. Triplex-forming oligonucleotide (TFO) treatment combined with Puromycin could efficiently suppress the growth of cell populations with DNA amplification. Similar observations in human cancer cell lines suggest that TFOs could be broadly applicable to mitigate drug resistance, one of the major difficulties in treating cancer.
耐药性继续阻碍癌症治疗的成功,因此需要建立广泛而简单的实验模型系统,以鉴定适用于多种癌症类型的机制和新对策。为了满足这些需求,我们研究了一组经过基因工程改造的哺乳动物细胞系,这些细胞系的基因组中整合了合成基因回路,以对嘌呤霉素产生抗性。我们发现,在 6 个重复群体中的 4 个群体中,DNA 扩增是耐药性的机制。三链形成寡核苷酸(TFO)与嘌呤霉素联合处理可以有效地抑制具有 DNA 扩增的细胞群体的生长。在人类癌细胞系中的类似观察表明,TFO 可广泛用于减轻耐药性,这是治疗癌症的主要困难之一。