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肥胖的炎症微环境可能会促进乳腺DCIS的进展

Ola Habanjar¹, Rawan Nehme¹, Nicolas Goncalves-Mendes¹

¹Université Clermont-Auvergne, INRAE, UNH, Clermont-Ferrand, France.

Frontiers in immunology

|July 29, 2024

概括

肥胖引起的脂肪组织炎症通过改变脂肪细胞和巨细胞的行为来促进乳腺癌的进展,阻碍保护性肌皮细胞. 这突显了脂肪组织在癌症发展中的关键作用.

科学领域:

乳腺癌研究研究乳腺癌研究
瘤微环境是一个微环境.
脂肪组织生物学脂肪组织生物学

背景情况:

在位管道癌 (DCIS) 是一种非侵入性乳腺癌.
肥胖及其相关的炎症性脂肪微环境可能会推动DCIS进展到侵入性导管癌 (IDC).
了解DCIS细胞,肌皮细胞 (MEC) 和脂肪微环境之间的相互作用至关重要.

研究的目的:

研究炎症性脂肪微环境对DCIS进展的影响.
评估DCIS细胞,MECs,脂肪细胞和巨细胞之间的相互作用.

主要方法:

使用DCIS类型的瘤,脂肪细胞和巨细胞开发3D共同培养模型.
在炎症性和非炎症性脂肪微环境中对瘤状行为进行比较.
分析瘤细胞,脂肪细胞和巨细胞中的基因表达.

主要成果:

炎症条件促进了癌细胞生存和入侵基因,同时抑制了亡基因.
MECs的保护功能受到损害.
肥胖脂肪细胞表现出肌纤维细胞关联基因表达 (myoCAFs),而体重正常的脂肪细胞显示出炎性纤维细胞表型 (iCAF);两者都影响了巨细胞两极分化.

结论:

瘤体和脂肪微环境之间的相互相互作用,特别是在肥胖症中,推动了乳腺癌的进展.
这些相互作用破坏了MEC层的完整性.
脂肪组织在乳腺癌的进展中起着重要作用.

关键词:

管道癌 in situ 的情况.这是一种炎症炎症炎症炎症.巨细胞是什么?巨细胞是什么?微环境是一个微环境.肌上皮细胞是肌上皮细胞.肥胖肥胖肥胖肥胖肥胖肥胖肥胖肥胖这是一种瘤性瘤.

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