Sensitivity to platinum-based combination chemotherapy is associated with a favorable prognosis in patients with non-small cell lung cancer (NSCLC). 近年来的研究显示，对于非小细胞肺癌（NSCLC）患者而言，对铂类联合化疗的敏感性与良好预后有关。 Here, our results obtained from analyses of the Gene Expression Omnibus database of NSCLC patients showed that cartilage acidic protein 1 (CRTAC1) plays a role in the response to platinum-based chemotherapy. 本研究利用对非小细胞肺癌（NSCLC）患者的基因表达库(Gene Expression Omnibus)进行分析，结果表明，软骨酸性蛋白1 (CRTAC1) 在对铂类化疗的反应中起到一定作用。 Overexpression of CRTAC1 increased sensitivity to cisplatin in vitro, whereas knockdown of CRTAC1 decreased chemosensitivity of NSCLC cells. 过表达CRTAC1在体外增加了对顺铂的敏感性，而CRTAC1的沉默则减弱了非小细胞肺癌细胞的化疗敏感性。 In vivo mouse experiments showed that CRTAC1 overexpression increased the antitumor effects of cisplatin. 通过体内小鼠实验，结果显示，CRTAC1的过表达增强了顺铂的抗肿瘤效果。 CRTAC1 overexpression promoted NFAT transcriptional activation by increasing intracellular Ca2+ levels, thereby inducing its regulated STUB1 mRNA transcription and protein expression, accelerating Akt1 protein degradation and, in turn, enhancing cisplatin-induced apoptosis. CRTAC1的过表达通过提高细胞内的Ca2+水平来促进NFAT转录活化，从而诱导其受控的STUB1 mRNA转录和蛋白质表达，加速Akt1蛋白降解，从而增强顺铂诱导的细胞凋亡。 Taken together, the present results indicate that CRTAC1 overexpression increases the chemosensitivity of NSCLC to cisplatin treatment by inducing Ca2+-dependent Akt1 degradation and apoptosis, suggesting the potential of CRTAC1 as a biomarker for predicting cisplatin chemosensitivity. 综上所述，本研究结果表明，CRTAC1过表达通过诱导依赖于Ca2+的Akt1降解和细胞凋亡来增加NSCLC对顺铂治疗的化疗敏感性，提示CRTAC1作为预测顺铂化疗敏感性的生物标志物的潜力。 Our results further reveal that modulating the expression of CRTAC1 could be a new strategy for increasing the efficacy of cisplatin in chemotherapy of NSCLC patients. 我们的研究进一步揭示，调节CRTAC1的表达可能是增加非小细胞肺癌患者顺铂化疗效果的一种新策略。 © 2023. The Author(s). 2023年版权归作者所有。

Sensitivity to platinum-based combination chemotherapy is associated with a favorable prognosis in patients with non-small cell lung cancer (NSCLC). Here, our results obtained from analyses of the Gene Expression Omnibus database of NSCLC patients showed that cartilage acidic protein 1 (CRTAC1) plays a role in the response to platinum-based chemotherapy. Overexpression of CRTAC1 increased sensitivity to cisplatin in vitro, whereas knockdown of CRTAC1 decreased chemosensitivity of NSCLC cells. In vivo mouse experiments showed that CRTAC1 overexpression increased the antitumor effects of cisplatin. CRTAC1 overexpression promoted NFAT transcriptional activation by increasing intracellular Ca2+ levels, thereby inducing its regulated STUB1 mRNA transcription and protein expression, accelerating Akt1 protein degradation and, in turn, enhancing cisplatin-induced apoptosis. Taken together, the present results indicate that CRTAC1 overexpression increases the chemosensitivity of NSCLC to cisplatin treatment by inducing Ca2+-dependent Akt1 degradation and apoptosis, suggesting the potential of CRTAC1 as a biomarker for predicting cisplatin chemosensitivity. Our results further reveal that modulating the expression of CRTAC1 could be a new strategy for increasing the efficacy of cisplatin in chemotherapy of NSCLC patients.© 2023. The Author(s).