Ovarian cancer (OC) is one of prevalent tumors and this study aimed to explore CCL20's effects on doxorubicin resistance of OC and related mechanisms. Doxorubicin-resistant SKOV3 DR cells were established from SKOV3 cells via 6-month continuous exposure to gradient concentrations of doxorubicin. Quantitative PCR and Western blot assay showed that SKOV3 DR cells had higher level of CCL20 than SKOV3 cells, and doxorubicin upregulated CCL20 expression in SKOV3 cells. MTT and cell count assay found that CCL20 overexpression plasmid enhanced doxorubicin resistance of SKOV3 and OVCA433 cells compared to empty vector, as shown by the increase in cell viability. In contrast, CCL20 shRNA enhanced doxorubicin sensitivity of SKOV3 DR cells compared to control. CCL20 overexpression plasmid promoted NF-kB activation and positively regulated ABCB1 expression. Besides, ABCB1 overexpression plasmid enhanced the viability of SKOV3 and OVCA433 cells compared to empty vector under treatment with the same concentration of doxorubicin, whereas ABCB1 shRNA inhibited doxorubicin resistance of SKOV3 DR cells compared to control. In conclusion, CCL20 enhanced doxorubicin resistance of OC cells by regulating ABCB1 expression.Key words: CCL20, ovarian cancer, doxorubicin resistance, tumor-promoting, ABCB1.

中文翻译：

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CCL20通过调节ABCB1表达促进卵巢癌化疗耐药。

卵巢癌（OC）是一种常见的肿瘤，该研究旨在探讨CCL20对OC对阿霉素耐药性的影响及其相关机制。通过连续6个月连续暴露于阿霉素梯度浓度，从SKOV3细胞建立耐阿霉素的SKOV3 DR细胞。定量PCR和Western印迹分析表明，SKOV3 DR细胞比SKOV3细胞具有更高的CCL20水平，并且阿霉素上调了SKOV3细胞中CCL20的表达。MTT和细胞计数分析发现，与空载体相比，CCL20过表达质粒增强了SKOV3和OVCA433细胞对阿霉素的抗性，如细胞活力的增加所证明。相反，与对照相比，CCL20 shRNA增强了SKOV3 DR细胞对阿霉素的敏感性。CCL20过表达质粒促进NF-kB激活并正向调节ABCB1表达。此外，与用相同浓度的阿霉素处理的空载体相比，ABCB1过表达质粒增强了SKOV3和OVCA433细胞的活力，而与对照相比，ABCB1 shRNA抑制了SKOV3 DR细胞对阿霉素的抗性。总之，CCL20通过调节ABCB1的表达来增强OC细胞对阿霉素的抗性。关键词：CCL20，卵巢癌，阿霉素抗性，促肿瘤，ABCB1。