Xu Quanxiao, Yu Jinsong, Jia Guangwei, Li Zhong, Xiong Hui
Department of Oncology, Nanyang First People's Hospital Affiliated to Henan University, Nanyang 473004, China.
Department of Thyroid and Breast Surgery, Nanyang First People's Hospital Affiliated to Henan University, Nanyang 473004, China; Key Laboratory of Thyroid Tumor Prevention and Treatment of Nanyang, Nanyang First People's Hospital Affiliated to Henan University, Nanyang 473004, China.
Cytokine. 2022 Jun;154:155888. doi: 10.1016/j.cyto.2022.155888. Epub 2022 Apr 18.
Breast cancer (BC) is the most commonly diagnosed cancer confronting women worldwide. Crocin, a glycosylated carotenoid extracted from Crocus sativus L., possesses anti-cancer and anti-inflammatory activities. This study tried to explore the influences of crocin on proliferation and inflammation of BC cells, and to investigate the possible mechanism. The protein levels of protein kinase C theta (PRKCQ) and nuclear factor kappa B (NF-κB) p-p65 and p65 were examined using western blot analysis. The potential targets of crocin were predicted using the PharmMapper database. Cell viability and proliferation were determined utilizing CCK-8 and EdU incorporation assays, respectively. Inflammation was assessed by detecting the levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) using RT-qPCR and ELISA. Results showed that crocin inhibited NF-κB activation and suppressed cell viability and proliferation in BC cells. Crocin caused a significant reduction of levels of TNF-α and IL-1β, suggesting that crocin suppressed inflammation in BC cells. NF-κB inhibition decreased proliferation and inflammation in BC cells. Additionally, PRKCQ was identified as a potential target of crocin according to PharmMapper database. Crocin treatment inhibited the activation of NF-κB in BC cells by reducing PRKCQ expression. Mechanistically, PRKCQ-dependent activation of NF-κB pathway reversed the effects of crocin on the proliferation and inflammation in BC cells. In conclusion, crocin inhibited NF-κB-mediated inflammation and proliferation in BC cells through reducing PRKCQ expression.
乳腺癌（BC）是全球女性中最常被诊断出的癌症。藏红花素是从番红花中提取的一种糖基化类胡萝卜素，具有抗癌和抗炎活性。本研究试图探讨藏红花素对BC细胞增殖和炎症的影响，并研究其可能的机制。采用蛋白质印迹分析检测蛋白激酶Cθ（PRKCQ）、核因子κB（NF-κB）的磷酸化p65和p65的蛋白水平。利用PharmMapper数据库预测藏红花素的潜在靶点。分别采用CCK-8和EdU掺入试验测定细胞活力和增殖情况。通过实时定量聚合酶链反应（RT-qPCR）和酶联免疫吸附测定（ELISA）检测肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）水平来评估炎症。结果表明，藏红花素抑制NF-κB激活，并抑制BC细胞的活力和增殖。藏红花素使TNF-α和IL-1β水平显著降低，表明藏红花素抑制BC细胞炎症。抑制NF-κB可降低BC细胞的增殖和炎症。此外，根据PharmMapper数据库，PRKCQ被确定为藏红花素的潜在靶点。藏红花素处理通过降低PRKCQ表达抑制BC细胞中NF-κB的激活。机制上，PRKCQ依赖的NF-κB途径激活逆转了藏红花素对BC细胞增殖和炎症的影响。总之，藏红花素通过降低PRKCQ表达抑制BC细胞中NF-κB介导的炎症和增殖。
