C1ql4通过PI3K/AKT/NF-κB信号通路调节乳腺癌细胞干细胞和上皮细胞-介质细胞过渡
Fan Xu1,2, Jiali Wang1, Shuman Zhen1
1Department of Tumor Immunotherapy, Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Frontiers in oncology
|June 16, 2023
概括
补充C1q-like 4 (C1ql4) 通过激活PI3K/AKT/NF-κB信号来促进乳腺癌的干细胞和转移. 准C1ql4可能为乳腺癌患者提供新的治疗策略.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 癌症研究 癌症研究
背景情况:
- 乳腺癌 (BC) 的干部驱动复发和转移.
- 了解乳腺癌干细胞 (BCSCs) 是改善患者治疗结果的关键.
研究的目的:
- 研究乳腺癌中补充C1q-like 4 (C1ql4) 的表达和临床意义.
- 阐明C1ql4在乳腺癌干和转移中的作用.
主要方法:
- 对临床BC标本进行了C1ql4表达的分析.
- 进行了西斑,qRT-PCR,流细胞计,伤口愈合和Transwell测试.
- 在体内研究中使用裸体小鼠瘤模型.
主要成果:
- 在BC组织和BCSC中,C1ql4的表达很高,与恶性瘤相关.
- C1ql4敲击抑制了树干,EMT,迁移和入侵,同时促进了亡.
- C1ql4激活PI3K/AKT/NF-κB信号传递,包括TNF-α和IL-1β.
结论:
- C1ql4通过PI3K/AKT/NF-κB信号传递促进BC干和上皮层-介质细胞过渡 (EMT).
- C1ql4代表了乳腺癌治疗的潜在治疗标.
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