دورية أكاديمية
أعرض في EDS

Bevacizumab Augments the Antitumor Efficacy of Infigratinib in Hepatocellular Carcinoma.

التفاصيل البيبلوغرافية
العنوان: Bevacizumab Augments the Antitumor Efficacy of Infigratinib in Hepatocellular Carcinoma.
المؤلفون: Le TBU; Department of Haematology-Oncology, National University Health System, Singapore 119074, Singapore., Vu TC; Laboratory of Molecular Endocrinology, Division of Molecular and Cellular Research, National Cancer Centre, Singapore 169610, Singapore., Ho RZW; Laboratory of Molecular Endocrinology, Division of Molecular and Cellular Research, National Cancer Centre, Singapore 169610, Singapore., Prawira A; Laboratory of Molecular Endocrinology, Division of Molecular and Cellular Research, National Cancer Centre, Singapore 169610, Singapore., Wang L; Department of Haematology-Oncology, National University Health System, Singapore 119074, Singapore.; Cancer Science Institute of Singapore, National University Hospital, Singapore 117599, Singapore., Goh BC; Department of Haematology-Oncology, National University Health System, Singapore 119074, Singapore.; Cancer Science Institute of Singapore, National University Hospital, Singapore 117599, Singapore., Huynh H; Laboratory of Molecular Endocrinology, Division of Molecular and Cellular Research, National Cancer Centre, Singapore 169610, Singapore.
المصدر: International journal of molecular sciences [Int J Mol Sci] 2020 Dec 10; Vol. 21 (24). Date of Electronic Publication: 2020 Dec 10.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: MDPI Country of Publication: Switzerland NLM ID: 101092791 Publication Model: Electronic Cited Medium: Internet ISSN: 1422-0067 (Electronic) Linking ISSN: 14220067 NLM ISO Abbreviation: Int J Mol Sci Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Basel, Switzerland : MDPI, [2000-
مواضيع طبية MeSH: Angiogenesis Inhibitors/*therapeutic use , Antineoplastic Agents, Immunological/*therapeutic use , Bevacizumab/*therapeutic use , Carcinoma, Hepatocellular/*drug therapy , Liver Neoplasms/*drug therapy , Phenylurea Compounds/*therapeutic use , Pyrimidines/*therapeutic use, Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Angiogenesis Inhibitors/administration & dosage ; Animals ; Antineoplastic Agents, Immunological/administration & dosage ; Apoptosis ; Bevacizumab/administration & dosage ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Drug Synergism ; Extracellular Signal-Regulated MAP Kinases/genetics ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Male ; Mice ; Mice, SCID ; Neoplasm Metastasis ; Phenylurea Compounds/administration & dosage ; Pyrimidines/administration & dosage ; Ribosomal Protein S6 Kinases, 70-kDa/genetics ; Ribosomal Protein S6 Kinases, 70-kDa/metabolism ; Survivin/genetics ; Survivin/metabolism ; Tumor Hypoxia ; cdc25 Phosphatases/genetics ; cdc25 Phosphatases/metabolism
مستخلص: The fibroblast growth factor (FGF) signaling cascade is one of the key signaling pathways in hepatocellular carcinoma (HCC). FGF has been shown to augment vascular endothelial growth factor (VEGF)-mediated HCC development and angiogenesis, as well as to potentially lead to resistance to VEGF/VEGF receptor (VEGFR)-targeted agents. Thus, novel agents targeting FGF/FGF receptor (FGFR) signaling may enhance and/or overcome de novo or acquired resistance to VEGF-targeted agents in HCC. Mice bearing high- and low-FGFR tumors were treated with Infigratinib (i.e., a pan-FGFR kinase inhibitor) and/or Bevacizumab (i.e., an angiogenesis inhibitor). The antitumor activity of both agents was assessed individually or in combination. Tumor vasculature, intratumoral hypoxia, and downstream targets of FGFR signaling pathways were also investigated. Infigratinib, when combined with Bevacizumab, exerted a synergistic inhibitory effect on tumor growth, invasion, and lung metastasis, and it significantly improved the overall survival of mice bearing FGFR-dependent HCC. Infigratinib/Bevacizumab promoted apoptosis, inhibited cell proliferation concomitant with upregulation of p27, and reduction in the expression of FGFR2-4, p-FRS-2, p-ERK1/2, p-p70S6K/4EBP1, Cdc25C, survivin, p-Cdc2, and p-Rb. Combining Infigratinib/Bevacizumab may provide therapeutic benefits for a subpopulation of HCC patients with FGFR-dependent tumors. A high level of FGFR-2/3 may serve as a potential biomarker for patient selection to Infigratinib/Bevacizumab.
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معلومات مُعتمدة: NMRC/MOHIAFCAT2/006/2016 Singapore National Medical Research Council; CGAug16M005 RIE2020 NCIS Centre Grant; NRF-CRP17-2017-05 National Research Foundation Singapore
فهرسة مساهمة: Keywords: angiogenesis inhibitor; growth inhibition; hepatocellular carcinoma; hypoxia; invasion; pan-FGFR inhibitor; vessel normalization
المشرفين على المادة: 0 (Adaptor Proteins, Signal Transducing)
0 (Angiogenesis Inhibitors)
0 (Antineoplastic Agents, Immunological)
0 (Cell Cycle Proteins)
0 (Eif4ebp1 protein, mouse)
0 (Phenylurea Compounds)
0 (Pyrimidines)
0 (Survivin)
2S9ZZM9Q9V (Bevacizumab)
A4055ME1VK (infigratinib)
EC 2.7.11.1 (Ribosomal Protein S6 Kinases, 70-kDa)
EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
EC 3.1.3.48 (Cdc25c protein, mouse)
EC 3.1.3.48 (cdc25 Phosphatases)
تواريخ الأحداث: Date Created: 20201216 Date Completed: 20210304 Latest Revision: 20210304
رمز التحديث: 20240829
مُعرف محوري في PubMed: PMC7764786
DOI: 10.3390/ijms21249405
PMID: 33321903
قاعدة البيانات: MEDLINE
الوصف
تدمد:1422-0067
DOI:10.3390/ijms21249405