دورية أكاديمية
أعرض في EDS

KAT7 serves as an oncogenic gene and regulates CCL3 expression via STAT1 signaling in osteosarcoma.

التفاصيل البيبلوغرافية
العنوان: KAT7 serves as an oncogenic gene and regulates CCL3 expression via STAT1 signaling in osteosarcoma.
المؤلفون: Yuan Q; Department of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, Jiangsu Province, People's Republic of China., Wu Y; Department of Orthopedics, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221006, Jiangsu Province, People's Republic of China., Xue C; Department of Orthopedics, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221006, Jiangsu Province, People's Republic of China., Zhao D; Department of Orthopedics, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221006, Jiangsu Province, People's Republic of China., Wang H; Department of Orthopedics, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221006, Jiangsu Province, People's Republic of China., Shen Y; Department of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, Jiangsu Province, People's Republic of China. Electronic address: 972679925@qq.com.
المصدر: Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2024 Aug 30; Vol. 722, pp. 150156. Date of Electronic Publication: 2024 May 23.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Elsevier Country of Publication: United States NLM ID: 0372516 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1090-2104 (Electronic) Linking ISSN: 0006291X NLM ISO Abbreviation: Biochem Biophys Res Commun Subsets: MEDLINE
أسماء مطبوعة: Publication: <2002- >: San Diego, CA : Elsevier
Original Publication: New York, Academic Press.
مواضيع طبية MeSH: Bone Neoplasms*/genetics , Bone Neoplasms*/metabolism , Bone Neoplasms*/pathology , Chemokine CCL3*/metabolism , Chemokine CCL3*/genetics , Gene Expression Regulation, Neoplastic* , Histone Acetyltransferases*/metabolism , Histone Acetyltransferases*/genetics , Osteosarcoma*/genetics , Osteosarcoma*/metabolism , Osteosarcoma*/pathology , Signal Transduction* , STAT1 Transcription Factor*/metabolism , STAT1 Transcription Factor*/genetics, Animals ; Humans ; Mice ; Cell Line, Tumor ; Cell Proliferation/genetics ; Mice, Nude
مستخلص: Osteosarcoma, considered as the primary cause of malignant bone tumors in children, necessitates novel therapeutic strategies to enhance overall survival rates. KAT7, a histone acetyltransferase, exerts pivotal functions in gene transcription and immune modulation. In light of this, our study identified a significant upregulation of KAT7 in the mRNA and protein levels in human osteosarcoma, boosting cell proliferation in vivo and in vitro. In addition, KAT7-mediated H3K14ac activation induced MMP14 transcription, leading to increased expression and facilitation of osteosarcoma cell metastasis. Subsequent bioinformatics analyses highlighted a correlation between KAT7 and adaptive immune responses, indicating CCL3 as a downstream target of KAT7. Mechanistically, STAT1 was found to transcriptionally upregulate CCL3 expression. Furthermore, overexpression of KAT7 suppressed CCL3 secretions, whereas knockdown of KAT7 enhanced its release. Overall, these findings underscore the oncogenic role of KAT7 in regulating immune responses for osteosarcoma treatment.
Competing Interests: Declaration of competing interest The authors declare no potential conflicts of interest.
(Copyright © 2024 Elsevier Inc. All rights reserved.)
فهرسة مساهمة: Keywords: CCL3; Immunity; KAT7; Osteosarcoma; STAT1 signal pathways
المشرفين على المادة: 0 (CCL3 protein, human)
0 (Chemokine CCL3)
EC 2.3.1.48 (Histone Acetyltransferases)
0 (STAT1 protein, human)
0 (STAT1 Transcription Factor)
EC 2.3.1.48 (KAT7 protein, human)
تواريخ الأحداث: Date Created: 20240526 Date Completed: 20240614 Latest Revision: 20240621
رمز التحديث: 20240622
DOI: 10.1016/j.bbrc.2024.150156
PMID: 38797155
قاعدة البيانات: MEDLINE
الوصف
تدمد:1090-2104
DOI:10.1016/j.bbrc.2024.150156