CYR61 confers chemoresistance by upregulating survivin expression in triple-negative breast cancer.

IF 3.3 3区 医学 Q2 ONCOLOGY
Hyungjoo Kim, Seogho Son, Yunhyo Ko, Hogeun Lim, Joohyung Lee, Kyung-Min Lee, Incheol Shin
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引用次数: 0

Abstract

Cysteine-rich angiogenic inducer 61 (CYR61) is a protein from the CCN family of matricellular proteins that play diverse regulatory roles in the extracellular matrix. CYR61 is involved in cell adhesion, migration, proliferation, differentiation, apoptosis, and senescence. Here, we show that CYR61 induces chemoresistance in triple-negative breast cancer (TNBC). We observed that CYR61 is overexpressed in TNBC patients, and CYR61 expression correlates negatively with the survival of patients who receive chemotherapy. CYR61 knockdown reduced cell migration, sphere formation and the cancer stem cell (CSC) population and increased the chemosensitivity of TNBC cells. Mechanistically, CYR61 activated Wnt/β-catenin signaling and increased survivin expression, which are associated with chemoresistance, the epithelial-mesenchymal transition, and CSC-like phenotypes. Altogether, our study demonstrates a novel function of CYR61 in chemotherapy resistance in breast cancer.

CYR61通过上调三阴性乳腺癌中存活素的表达而产生化疗耐药性。
富半胱氨酸血管生成诱导剂 61(CYR61)是一种属于 CCN 家族的基质蛋白,在细胞外基质中发挥着多种调节作用。CYR61 参与细胞粘附、迁移、增殖、分化、凋亡和衰老。在这里,我们发现 CYR61 会诱导三阴性乳腺癌(TNBC)的化疗耐药性。我们观察到 CYR61 在 TNBC 患者中过表达,而且 CYR61 的表达与接受化疗的患者的生存率呈负相关。敲除 CYR61 可减少细胞迁移、球体形成和癌症干细胞(CSC)数量,并增加 TNBC 细胞的化疗敏感性。从机理上讲,CYR61激活了Wnt/β-catenin信号转导并增加了survivin的表达,这与化疗耐药性、上皮-间质转化和CSC样表型有关。总之,我们的研究证明了 CYR61 在乳腺癌化疗耐药性中的新功能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Carcinogenesis
Carcinogenesis 医学-肿瘤学
CiteScore
9.20
自引率
2.10%
发文量
95
审稿时长
1 months
期刊介绍: Carcinogenesis: Integrative Cancer Research is a multi-disciplinary journal that brings together all the varied aspects of research that will ultimately lead to the prevention of cancer in man. The journal publishes papers that warrant prompt publication in the areas of Biology, Genetics and Epigenetics (including the processes of promotion, progression, signal transduction, apoptosis, genomic instability, growth factors, cell and molecular biology, mutation, DNA repair, genetics, etc.), Cancer Biomarkers and Molecular Epidemiology (including genetic predisposition to cancer, and epidemiology), Inflammation, Microenvironment and Prevention (including molecular dosimetry, chemoprevention, nutrition and cancer, etc.), and Carcinogenesis (including oncogenes and tumor suppressor genes in carcinogenesis, therapy resistance of solid tumors, cancer mouse models, apoptosis and senescence, novel therapeutic targets and cancer drugs).
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