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在三阴性乳腺癌中,B细胞增强了IL-1β驱动的侵入性

Nicole J Toney^1,2, Lynn M Opdenaker¹, Lisa Frerichs¹

¹Cawley Center for Translational Cancer Research, Helen F. Graham Cancer Center and Research Institute Christiana Care Health Services, Inc., 4701 Ogletown Stanton Rd Suite 4300, Newark, DE, 19713, USA.

Scientific reports

|January 17, 2025

概括

在三阴性乳腺癌 (TNBC) 中,瘤透的B细胞通过NFκB信号传递来增加Interleukin-1β (IL-1β),从而促进侵袭和迁移. IL-1 抑制剂可能为早期和侵入性TNBC提供新的治疗选择.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

三阴性乳腺癌 (TNBC) 是具有攻击性的,通常具有显著的淋巴细胞透,包括瘤透B细胞 (TIBs).
即使在TNBC的早期阶段也观察到TIB,并且与微侵袭有关,这表明TIB在疾病进展中的早期作用.

研究的目的:

研究B细胞在TNBC进展中的功能作用.
阐明TIBs影响TNBC入侵和迁移的分子机制.
评估TNBC不同阶段的干白素-1β (IL-1β) 和TIBs的临床相关性.

主要方法:

与B细胞共同培养TNBC细胞,以评估IL-1β的表达和分泌.
对NFκB信号通路激活的分析.
测量矩阵金属蛋白酶 (MMP) 活动,入侵和迁移.
在本位导管癌 (DCIS) 和侵入性TNBC患者样本中对IL-1β和TIB进行免疫组织化学分析.

主要成果:

同时培养TNBC和B细胞显著增加IL-1β的表达和分泌.
B细胞诱导的IL-1β激活了NFκB信号,导致MMP活动,入侵和迁移的增加.
在DCIS中,TIB与IL-1β和微侵袭相关;IL-1β与复发有关.
在侵袭性TNBC中,IL-1β与TIB密度和阶段相关,高IL-1β与较差的生存率相关.

结论:

早期B细胞透到TNBC可以驱动IL-1β分泌,通过IL-1β-NFκB通路促进癌细胞的入侵和迁移.
IL-1β和TIBs是TNBC中重要的生物标志物,与疾病进展和患者的结果相关.
IL-1 抑制剂代表了对荷尔蒙受体阴性DCIS和TNBC的潜在治疗策略.

关键词:

B 细胞 B 细胞 B 细胞乳腺癌乳腺癌乳腺癌互乐金1ββ的存在 NFkappa B BFkappa B 这是一个很好的选择.三重阴性乳腺癌是什么?

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