دورية أكاديمية
أعرض في EDS

Chemotherapy-Induced Collagen IV Drives Cancer Cell Motility through Activation of Src and Focal Adhesion Kinase.

التفاصيل البيبلوغرافية
العنوان: Chemotherapy-Induced Collagen IV Drives Cancer Cell Motility through Activation of Src and Focal Adhesion Kinase.
المؤلفون: Fatherree JP; Department of Biomedical Engineering, Tufts School of Engineering, Tufts University, Medford, Massachusetts., Guarin JR; Department of Biomedical Engineering, Tufts School of Engineering, Tufts University, Medford, Massachusetts., McGinn RA; Department of Biomedical Engineering, Tufts School of Engineering, Tufts University, Medford, Massachusetts., Naber SP; Department of Pathology and Laboratory Medicine, Tufts Medical Center, Boston, Massachusetts., Oudin MJ; Department of Biomedical Engineering, Tufts School of Engineering, Tufts University, Medford, Massachusetts.
المصدر: Cancer research [Cancer Res] 2022 May 16; Vol. 82 (10), pp. 2031-2044.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: American Association for Cancer Research Country of Publication: United States NLM ID: 2984705R Publication Model: Print Cited Medium: Internet ISSN: 1538-7445 (Electronic) Linking ISSN: 00085472 NLM ISO Abbreviation: Cancer Res Subsets: MEDLINE
أسماء مطبوعة: Publication: Baltimore, Md. : American Association for Cancer Research
Original Publication: Chicago [etc.]
مواضيع طبية MeSH: Antineoplastic Agents*/pharmacology , Antineoplastic Agents*/therapeutic use , Triple Negative Breast Neoplasms*/pathology, Animals ; Anthracyclines ; Cell Movement ; Collagen Type IV ; Focal Adhesion Protein-Tyrosine Kinases ; Humans ; Mice ; Taxoids/therapeutic use
مستخلص: Triple-negative breast cancer (TNBC) is the most aggressive and deadly subtype of breast cancer, accounting for 30,000 cases annually in the United States. While there are several clinical trials ongoing to identify new agents to treat TNBC, the majority of patients with TNBC are treated with anthracycline- or taxane-based chemotherapies in the neoadjuvant setting, followed by surgical resection and adjuvant chemotherapy. While many patients respond well to this approach, as many as 25% will suffer local or metastatic recurrence within 5 years. Understanding the mechanisms that drive recurrence after chemotherapy treatment is critical to improving survival for patients with TNBC. It is well established that the extracellular matrix (ECM), which provides structure and support to tissues, is a major driver of tumor growth, local invasion, and dissemination of cancer cells to distant metastatic sites. In the present study, we show that decellularized ECM (dECM) obtained from chemotherapy-treated mice increases motility of treatment-naïve breast cancer cells compared with vehicle-treated dECM. Tandem-mass-tag proteomics revealed that anthracycline- and taxane-based chemotherapies induce drug-specific changes in tumor ECM composition. The basement membrane protein collagen IV was significantly upregulated in the ECM of chemotherapy-treated mice and patients treated with neoadjuvant chemotherapy. Collagen IV drove invasion via activation of Src and focal adhesion kinase signaling downstream of integrin α1 and α2, and inhibition of collagen IV-driven signaling decreased motility in chemotherapy-treated dECM. These studies provide a novel mechanism by which chemotherapy may induce metastasis via its effects on ECM composition.
Significance: Cytotoxic chemotherapy induces significant changes in the composition of tumor ECM, inducing a more invasive and aggressive phenotype in residual tumor cells following chemotherapy.
(©2022 The Authors; Published by the American Association for Cancer Research.)
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معلومات مُعتمدة: R00 CA207866 United States CA NCI NIH HHS
المشرفين على المادة: 0 (Anthracyclines)
0 (Antineoplastic Agents)
0 (Collagen Type IV)
0 (Taxoids)
EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases)
تواريخ الأحداث: Date Created: 20220309 Date Completed: 20220517 Latest Revision: 20230106
رمز التحديث: 20230106
مُعرف محوري في PubMed: PMC9381104
DOI: 10.1158/0008-5472.CAN-21-1823
PMID: 35260882
قاعدة البيانات: MEDLINE
الوصف
تدمد:1538-7445
DOI:10.1158/0008-5472.CAN-21-1823