Kolosenko Iryna, Yu Yasmin, Busker Sander, Dyczynski Matheus, Liu Jianping, Haraldsson Martin, Palm Apergi Caroline, Helleday Thomas, Tamm Katja Pokrovskaja, Page Brent D G, Grander Dan
Cancer Center Karolinska, Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.
Karolinska High-Throughput Center, Department of Medical Biochemistry and Biophysics, Division of Functional Genomics, Karolinska Institutet Stockholm, Sweden.
PLoS One. 2017 Jun 21;12(6):e0178844. doi: 10.1371/journal.pone.0178844. eCollection 2017.
Activation of Signal Transducer and Activator of Transcription 3 (STAT3) has been linked to several processes that are critical for oncogenic transformation, cancer progression, cancer cell proliferation, survival, drug resistance and metastasis. Inhibition of STAT3 signaling has shown a striking ability to inhibit cancer cell growth and therefore, STAT3 has become a promising target for anti-cancer drug development. The aim of this study was to identify novel inhibitors of STAT-dependent gene transcription. A cellular reporter-based system for monitoring STAT3 transcriptional activity was developed which was suitable for high-throughput screening (Z' = 0,8). This system was used to screen a library of 28,000 compounds (the ENAMINE Drug-Like Diversity Set). Following counter-screenings and toxicity studies, we identified four hit compounds that were subjected to detailed biological characterization. Of the four hits, KI16 stood out as the most promising compound, inhibiting STAT3 phosphorylation and transcriptional activity in response to IL6 stimulation. In silico docking studies showed that KI16 had favorable interactions with the STAT3 SH2 domain, however, no inhibitory activity could be observed in the STAT3 fluorescence polarization assay. KI16 inhibited cell viability preferentially in STAT3-dependent cell lines. Taken together, using a targeted, cell-based approach, novel inhibitors of STAT-driven transcriptional activity were discovered which are interesting leads to pursue further for the development of anti-cancer therapeutic agents.
信号转导子与转录激活子3(STAT3)的激活与致癌转化、癌症进展、癌细胞增殖、存活、耐药性和转移等几个关键过程相关。抑制STAT3信号传导已显示出显著抑制癌细胞生长的能力,因此,STAT3已成为抗癌药物开发的一个有前景的靶点。本研究的目的是鉴定STAT依赖性基因转录的新型抑制剂。开发了一种基于细胞报告基因的系统来监测STAT3转录活性,该系统适用于高通量筛选(Z' = 0.8)。该系统用于筛选一个包含28000种化合物的文库(ENAMINE类药物多样性集)。经过反筛选和毒性研究,我们鉴定出了四种有活性的化合物,并对其进行了详细的生物学特性分析。在这四种有活性的化合物中,KI16是最有前景的化合物,它能抑制IL6刺激下的STAT3磷酸化和转录活性。计算机对接研究表明,KI16与STAT3的SH2结构域有良好的相互作用,然而,在STAT3荧光偏振分析中未观察到抑制活性。KI16优先抑制STAT3依赖性细胞系中的细胞活力。综上所述,通过一种有针对性的、基于细胞的方法,发现了STAT驱动转录活性的新型抑制剂,这些抑制剂是进一步开发抗癌治疗药物的有趣线索。