دورية أكاديمية

NKX2-1-AS1 promotes the lymphangiogenesis of lung adenocarcinoma through regulation of ERG-mediated FABP4.

التفاصيل البيبلوغرافية
العنوان: NKX2-1-AS1 promotes the lymphangiogenesis of lung adenocarcinoma through regulation of ERG-mediated FABP4.
المؤلفون: Tao T; Department of Pathology, the First Hospital of Changsha, Changsha, Hunan 410005, PR China., Chen H; Department of Pathology, the First Hospital of Changsha, Changsha, Hunan 410005, PR China., Xu Q; Department of Pathology, the First Hospital of Changsha, Changsha, Hunan 410005, PR China., Li Z; Department of Pathology, the First Hospital of Changsha, Changsha, Hunan 410005, PR China., Chen X; Department of Respiratory Medicine, the First Hospital of Changsha, Changsha, Hunan 410005, PR China., Zhou X; Department of Pathology, the First Hospital of Changsha, Changsha, Hunan 410005, PR China., Luo W; Laboratory Medicine, the First Hospital of Changsha, Changsha, Hunan 410005, PR China. Electronic address: lwluowu@163.com.
المصدر: Tissue & cell [Tissue Cell] 2024 Apr; Vol. 87, pp. 102314. Date of Electronic Publication: 2024 Jan 29.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Churchill Livingstone Country of Publication: Scotland NLM ID: 0214745 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1532-3072 (Electronic) Linking ISSN: 00408166 NLM ISO Abbreviation: Tissue Cell Subsets: MEDLINE
أسماء مطبوعة: Publication: Edinburgh : Churchill Livingstone
Original Publication: Edinburgh, Oliver & Boyd.
مواضيع طبية MeSH: Adenocarcinoma*/genetics , Lung Neoplasms*/genetics , Lung Neoplasms*/pathology , MicroRNAs*/genetics , RNA, Long Noncoding*/genetics, Humans ; Cell Line, Tumor ; Cell Proliferation/genetics ; Fatty Acid-Binding Proteins/genetics ; Fatty Acid-Binding Proteins/metabolism ; Gene Expression Regulation, Neoplastic ; Lung/pathology ; Lymphangiogenesis/genetics ; Transcriptional Regulator ERG/genetics ; Transcriptional Regulator ERG/metabolism
مستخلص: Lymphatic metastasis is a common metastasis of lung adenocarcinoma (LUAD). The current study illustrated the action of lncRNA NKX2-1-AS1 in lymphangiogenesis in LUAD and the underlying mechanisms. Clinical tissue samples were collected for determining NKX2-1-AS1 expression. Then, H441 and H661 cells were selected to perform gain- and loss-of-function assays for dissecting the roles of NKX2-1-AS1 in LUAD cell proliferation and migration. Besides, H441 and H661 cell supernatant was harvested to stimulate HLECs for assessing tube formation ability. Interaction among NKX2-1-AS1, ERG, and fatty acid binding protein 4 (FABP4) was validated through luciferase and RIP assays. NKX2-1-AS1 was highly-expressed in LUAD tissues. Silencing NKX2-1-AS1 suppressed H441 and H661 cell proliferation and migration, reduced expression levels of lymphangiogenesis-related factors (LYVE-1, VEGF-C, VEGFR3, VEGF-A, VEGFR2, and CCR7), and inhibited HLEC tube formation. Interaction validation demonstrated that NKX2-1-AS1 regulated FABP4 transcription by binding to ERG. Overexpression of FABP4 could effectively block the inhibition role of NKX2-1-AS1 silencing in lymphangiogenesis in H441 and H661 cells. This study provided evidence that NKX2-1-AS1 regulated FABP4 transcription by binding to ERG to facilitate the proliferation and migration of LUAD cells and tube formation of HLECs, thus participating in lymphangiogenesis.
Competing Interests: Declaration of Competing Interest The authors report no relationships that could be construed as a conflict of interest.
(Copyright © 2024 Elsevier Ltd. All rights reserved.)
فهرسة مساهمة: Keywords: ERG; FABP4; Lung adenocarcinoma; Lymphangiogenesis; NKX2–1-AS1; VEGF-C
المشرفين على المادة: 0 (ERG protein, human)
0 (FABP4 protein, human)
0 (Fatty Acid-Binding Proteins)
0 (MicroRNAs)
0 (RNA, Long Noncoding)
0 (Transcriptional Regulator ERG)
0 (NKX2-1 protein, human)
تواريخ الأحداث: Date Created: 20240203 Date Completed: 20240319 Latest Revision: 20240320
رمز التحديث: 20240320
DOI: 10.1016/j.tice.2024.102314
PMID: 38309204
قاعدة البيانات: MEDLINE
الوصف
تدمد:1532-3072
DOI:10.1016/j.tice.2024.102314