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抑制PI3K-AKT-mTOR信号通路可抑制脂肪细胞介导的乳腺癌细胞增殖和迁移。

Inhibition of the PI3K-AKT-mTOR pathway suppresses the adipocyte-mediated proliferation and migration of breast cancer cells.

作者信息

Park Jae-Yeo, Kang Shi-Eun, Ahn Kwang Seok, Um Jae-Young, Yang Woong Mo, Yun Miyong, Lee Seok-Geun

机构信息

Department of Science in Korean Medicine and Comorbidity Research Institute, Kyung Hee University, Seoul, Republic of Korea.

KHU-KIST department of Converging Science and Technology, Kyung Hee University, Seoul, Republic of Korea.

出版信息

J Cancer. 2020 Feb 10;11(9):2552-2559. doi: 10.7150/jca.37975. eCollection 2020.

DOI:10.7150/jca.37975
PMID:32201525
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7065999/
Abstract

: Although it is well known that adipocyte significantly affects breast cancer progression, its mechanism has not been fully understood. Here, we analyzed the effect of adipocytes on breast cancer progression including cell proliferation and migration. : We treated the conditioned media obtained from mouse 3T3-L1-derived or human adipose tissue-derived mesenchymal stem cells (hAMSC)-derived adipocytes to breast cancer cells, MCF-7 and MDA-MB-231. And then, cells viability and proliferation were analyzed using MTT assays and colony forming assays, respectively. Also mRNA expression of inflammatory cytokines and proteins expression in main signal pathway were analyzed by RT-qPCR and immunoblotting, respectively. : Adipocyte-derived conditioned media increased the proliferation and migration of MCF-7 and MDA-MB-231 cells while little effects in a human normal immortalized mammary epithelial cell line MCF10A. In addition, adipocyte-derived conditioned media induced phosphorylation of AKT and mTOR and upregulated the expression of target genes of the PI3K-AKT-mTOR pathway including IL6, IL1β, IL1α and TNFα in breast cancer cells. Furthermore, BEZ235 a dual inhibitor of PI3K and mTOR significantly decreased the adipocyte-mediated the proliferation and migration of breast cancer cells. : Adipocyte-derived conditioned media enhance the proliferation and migration of breast cancer cells through the PI3K-AKT-mTOR pathway, supporting the importance of heterotypic interactions between breast cancer cells and adipocytes in the tumor microenvironment.

摘要

虽然众所周知脂肪细胞会显著影响乳腺癌的进展，但其机制尚未完全阐明。在此，我们分析了脂肪细胞对乳腺癌进展的影响，包括细胞增殖和迁移。

我们将从小鼠3T3-L1来源或人脂肪组织来源的间充质干细胞（hAMSC）分化而来的脂肪细胞所获得的条件培养基作用于乳腺癌细胞MCF-7和MDA-MB-231。然后，分别使用MTT法和集落形成试验分析细胞活力和增殖情况。此外，还分别通过RT-qPCR和免疫印迹分析炎症细胞因子的mRNA表达以及主要信号通路中的蛋白表达。

脂肪细胞来源的条件培养基增加了MCF-7和MDA-MB-231细胞的增殖和迁移，而对人正常永生化乳腺上皮细胞系MCF10A影响较小。此外，脂肪细胞来源的条件培养基诱导乳腺癌细胞中AKT和mTOR的磷酸化，并上调PI3K-AKT-mTOR通路靶基因（包括IL6、IL1β、IL1α和TNFα）的表达。此外，PI3K和mTOR的双重抑制剂BEZ235显著降低了脂肪细胞介导的乳腺癌细胞增殖和迁移。

脂肪细胞来源的条件培养基通过PI3K-AKT-mTOR通路增强乳腺癌细胞的增殖和迁移，支持了肿瘤微环境中乳腺癌细胞与脂肪细胞之间异型相互作用的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70da/7065999/f7e00fc99675/jcav11p2552g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70da/7065999/64bf84497d3a/jcav11p2552g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70da/7065999/43ec54603e75/jcav11p2552g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70da/7065999/5148069c898c/jcav11p2552g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70da/7065999/f7e00fc99675/jcav11p2552g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70da/7065999/64bf84497d3a/jcav11p2552g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70da/7065999/43ec54603e75/jcav11p2552g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70da/7065999/5148069c898c/jcav11p2552g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70da/7065999/f7e00fc99675/jcav11p2552g004.jpg

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