دورية أكاديمية

CRKL but not CRKII contributes to hemin-induced erythroid differentiation of CML.

التفاصيل البيبلوغرافية
العنوان: CRKL but not CRKII contributes to hemin-induced erythroid differentiation of CML.
المؤلفون: Guo C; Department of Biotechnology & Liaoning Key Laboratory of Cancer Stem Cell Research, College of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning, China., Lv X; Department of Biotechnology & Liaoning Key Laboratory of Cancer Stem Cell Research, College of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning, China., Zhang Q; Department of Biochemistry, College of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning, China., Yi L; Department of Biochemistry, College of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning, China., Ren Y; Department of Biotechnology & Liaoning Key Laboratory of Cancer Stem Cell Research, College of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning, China., Li Z; Department of Biochemistry, College of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning, China., Yan J; Department of Hematology, The Second Affiliated Hospital of Dalian Medical University, Institute of Stem Cell Transplantation of Dalian Medical University, Dalian, Liaoning, China., Zheng S; Department of Biochemistry, College of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning, China., Sun MZ; Department of Biotechnology & Liaoning Key Laboratory of Cancer Stem Cell Research, College of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning, China., Liu S; Department of Biochemistry, College of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning, China.
المصدر: Journal of cellular and molecular medicine [J Cell Mol Med] 2024 May; Vol. 28 (9), pp. e18308.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Wiley-Blackwell Country of Publication: England NLM ID: 101083777 Publication Model: Print Cited Medium: Internet ISSN: 1582-4934 (Electronic) Linking ISSN: 15821838 NLM ISO Abbreviation: J Cell Mol Med Subsets: MEDLINE
أسماء مطبوعة: Publication: Oxford, England : Wiley-Blackwell
Original Publication: Bucharest : "Carol Davila" University Press, 2000-
مواضيع طبية MeSH: Adaptor Proteins, Signal Transducing*/metabolism , Adaptor Proteins, Signal Transducing*/genetics , Cell Differentiation*/drug effects , Erythroid Cells*/metabolism , Erythroid Cells*/drug effects , Erythroid Cells*/pathology , Erythroid Cells*/cytology , Hemin*/pharmacology , Leukemia, Myelogenous, Chronic, BCR-ABL Positive*/pathology , Leukemia, Myelogenous, Chronic, BCR-ABL Positive*/genetics , Leukemia, Myelogenous, Chronic, BCR-ABL Positive*/metabolism , MicroRNAs*/genetics , MicroRNAs*/metabolism , Proto-Oncogene Proteins c-crk*/metabolism , Proto-Oncogene Proteins c-crk*/genetics, Humans ; 3' Untranslated Regions ; Erythropoiesis/genetics ; Erythropoiesis/drug effects ; Gene Expression Regulation, Leukemic/drug effects ; K562 Cells ; MAP Kinase Signaling System/drug effects
مستخلص: Destruction of erythropoiesis process leads to various diseases, including thrombocytopenia, anaemia, and leukaemia. miR-429-CT10 regulation of kinase-like (CRKL) axis involved in development, progression and metastasis of cancers. However, the exact role of miR-429-CRKL axis in leukaemic cell differentiation are still unknown. The current work aimed to uncover the effect of miR-429-CRKL axis on erythropoiesis. In the present study, CRKL upregulation was negatively correlated with miR-429 downregulation in both chronic myeloid leukaemia (CML) patient and CR patient samples. Moreover, CRKL expression level was significantly decreased while miR-429 expression level was increased during the erythroid differentiation of K562 cells following hemin treatment. Functional investigations revealed that overexpression and knockdown of CRKL was remarkably effective in suppressing and promoting hemin-induced erythroid differentiation of K562 cells, whereas, miR-429 exhibited opposite effects to CRKL. Mechanistically, miR-429 regulates erythroid differentiation of K562 cells by downregulating CRKL via selectively targeting CRKL-3'-untranslated region (UTR) through Raf/MEK/ERK pathway. Conversely, CRKII had no effect on erythroid differentiation of K562 cells. Taken together, our data demonstrated that CRKL (but not CRKII) and miR-429 contribute to development, progression and erythropoiesis of CML, miR-429-CRKL axis regulates erythropoiesis of K562 cells via Raf/MEK/ERK pathway, providing novel insights into effective diagnosis and therapy for CML patients.
(© 2024 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)
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معلومات مُعتمدة: 31900517 National Natural Science Foundation of China
فهرسة مساهمة: Keywords: CML; Raf/MEK/ERK pathway; erythroid differentiation; miR‐429‐CRKL axis
المشرفين على المادة: 0 (3' Untranslated Regions)
0 (Adaptor Proteins, Signal Transducing)
0 (CRKL protein)
743LRP9S7N (Hemin)
0 (MicroRNAs)
0 (MIRN429 microRNA, human)
0 (Proto-Oncogene Proteins c-crk)
تواريخ الأحداث: Date Created: 20240429 Date Completed: 20240429 Latest Revision: 20240509
رمز التحديث: 20240509
مُعرف محوري في PubMed: PMC11057422
DOI: 10.1111/jcmm.18308
PMID: 38683131
قاعدة البيانات: MEDLINE
الوصف
تدمد:1582-4934
DOI:10.1111/jcmm.18308