國家衛生研究院 NHRI:Item 3990099045/13649
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    题名: CD44 inhibits DCIS progression to invasive carcinoma
    作者: Liu, F;Zhou, J;Kundu-Roy, T;Wahler, J;So, JY;Lin, Y;Lou, YR;Barnard, NJ;Matsuura, I;Suh, N
    贡献者: Institute of Molecular and Genomic Medicine
    摘要: Ductal carcinoma in situ (DCIS) transition to invasive tumor is an important issue for breast cancer. The human MCF10DCIS.com cell line (abbreviated as MCF10DCIS) is derived from the spontaneously immortalized human MCF10A breast epithelial cell line. The MCF10DCIS xenografts are similar to human high grade comedo DCIS. In the xenograft assay, MCF10DCIS cells form DCIS-like lesion, remain as DCIS-like lesion in the first several weeks, and then progress into invasive carcinoma. Thus, it is an excellent model to study human breast cancer transition from DCIS to invasive carcinoma. To the best of our knowledge, it is the most commonly used model for DCIS transition to invasive carcinoma. We investigated the role of CD44 in breast cancer transition from DCIS to invasive carcinoma by knockdown the expression of CD44 in the MCF10DCIS xenograft model. Our results show that knockdown of CD44 expression in the MCF10DCIS cells enhances DCIS transition to invasive carcinoma. Our finding is supported by a previous study which showed that CD44 expression was lower in invasive human breast carcinomas than in DCIS, especially in the luminal A subtype. Our study uncovered an unexpected role of CD44 in the inhibition of DCIS transition to invasive carcinoma. We will also present a model for the underlying mechanisms for the protective role of CD44 in the inhibition of transition from DCIS to invasive carcinoma. Our findings have important implications for breast cancer.
    日期: 2021-07
    關聯: Cancer Research. 2021 Jul;80(16, Suppl.):Abstract number 5052.
    Link to: https://doi.org/10.1158/1538-7445.AM2020-5052
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0008-5472&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000680263504252
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