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通过CSF3R/JAK2/STAT3正反循环,CSF3R-AS促进肝细胞癌的进展和索拉费尼布耐药性
Ziyang Feng1,2,3, Yan Gao1, Changjing Cai1
1Department of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
反意义圆形RNA CSF3R-AS通过稳定CSF3RmRNA和激活JAK2/STAT3通路来促进肝细胞癌 (HCC) 的生长和转移. 这种反循环也驱动HCC中的sorafenib耐药性.
科学领域:
- 分子生物学分子生物学
- 在瘤学瘤学.
- 在RNA生物学,RNA生物学.
背景情况:
- 反意义循环RNAs (circRNAs) 是基因表达的新兴调节者.
- 在肝细胞癌 (HCC) 中,反感性circRNAs的作用仍然在很大程度上未被探索.
研究的目的:
- 为了研究HCC.中反感性circRNA CSF3R-AS的功能.
- 阐明HCC的潜在分子机制和治疗潜力.
主要方法:
- 定量实时PCR用于评估CSF3R-AS表达式.
- 细胞增殖,血管生成和转移的测试.
- 西方模糊和光酶记者测试以调查信号通路.
主要成果:
- 在HCC组织中,CSF3R-AS显著上调,与预后不佳相关.
- CSF3R-AS促进了HCC细胞的增殖,血管新生和转移,同时抑制了细胞亡.
- CSF3R-AS直接与CSF3RmRNA结合,使其稳定并激活JAK2/STAT3通路,形成一个正反循环.
结论:
- 在CSF3R-AS/CSF3R/JAK2/STAT3正反循环驱动HCC的进展和 sorafenib抵抗.
- 准这种循环为治疗HCC和克服药物耐药性提供了潜在的治疗策略.
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