Circular RNAs have been shown to regulate cancer tumorigenesis and drug resistance. Recently, circCCND1 is reported to promote laryngeal squamous cell carcinoma; however, whether circCCND1 is implicated in non-small cell lung cancer (NSCLC) remains unclear. In this research, The Cancer Genome Atlas data of lung adenocarcinoma were analyzed to show gene expression and overall survival. 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide assay and cell colony formation assay were utilized to measure cell viability and proliferation of A549 and HCC827. Apoptosis was detected by TdT-mediated dUTP Nick-End Labeling assay. Besides, reverse transcription-quantitative PCR was used to examine gene expression. We observed that circCCND1 was significantly upregulated in lung cancer cells and patients. circCCND1 knockdown attenuated cell proliferation and induced apoptosis under cisplatin treatment. Mechanistically, circCCND1 interacted with miR-187-3p to regulate reactive oxygen species and FGF9 in NSCLC cells. Finally, miR-187-3p was demonstrated to rescue circCCND1 knockdown-modulated chemoresistance of NSCLC cells. In this study, our conclusions facilitate the understanding of NSCLC drug resistance to cisplatin.

中文翻译：

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circCCND1通过海绵化miR-187-3p调节氧化应激和FGF9增强非小细胞肺癌的化学耐药性

环状RNA已被证明可调节癌症的发生和耐药性。最近，有报道称circCCND1可促进喉鳞状细胞癌。但是，尚不清楚circCCND1是否与非小细胞肺癌（NSCLC）有关。在这项研究中，对肺腺癌的癌症基因组图谱数据进行了分析，以显示基因表达和总体存活率。利用3-（4,5）-二甲基噻唑偶氮（-z-y1）-3,5-二苯并四唑鎓溴化物测定和细胞集落形成测定来测量A549和HCC827的细胞活力和增殖。通过TdT介导的dUTP尼克末端标记测定法检测凋亡。此外，使用逆转录定量PCR检测基因表达。我们观察到circCCND1在肺癌细胞和患者中显着上调。在顺铂处理下，circCCND1敲低减弱了细胞的增殖并诱导了细胞凋亡。从机制上讲，circCCND1与miR-187-3p相互作用以调节NSCLC细胞中的活性氧和FGF9。最后，证明了miR-187-3p可以挽救circCCND1敲低调节的NSCLC细胞的化学耐药性。在这项研究中，我们的结论有助于理解NSCLC对顺铂的耐药性。