Informacja

Drogi użytkowniku, aplikacja do prawidłowego działania wymaga obsługi JavaScript. Proszę włącz obsługę JavaScript w Twojej przeglądarce.

Tytuł pozycji:

High expression levels of FANCI correlate with worse prognosis and promote tumor growth of lung adenocarcinoma partly via suppression of M1 macrophages.

Tytuł:
High expression levels of FANCI correlate with worse prognosis and promote tumor growth of lung adenocarcinoma partly via suppression of M1 macrophages.
Autorzy:
Li W; Shengli Clinical Medical College, Fujian Medical University, Fuzhou 350001, China; Department of Thoracic Surgery, Fujian Provincial Hospital, Fuzhou 350001, China.
Yu M; Shengli Clinical Medical College, Fujian Medical University, Fuzhou 350001, China; Department of Nuclear Medicine, Fujian Provincial Hospital, Fuzhou 350001, China.
Zhang J; Shengli Clinical Medical College, Fujian Medical University, Fuzhou 350001, China; Department of Thoracic Surgery, Fujian Provincial Hospital, Fuzhou 350001, China.
Huang J; Shengli Clinical Medical College, Fujian Medical University, Fuzhou 350001, China; Department of Thoracic Surgery, Fujian Provincial Hospital, Fuzhou 350001, China.
Lin Z; Shengli Clinical Medical College, Fujian Medical University, Fuzhou 350001, China; Department of Thoracic Surgery, Fujian Provincial Hospital, Fuzhou 350001, China.
Chen J; Shengli Clinical Medical College, Fujian Medical University, Fuzhou 350001, China; Department of Oncology, Fujian Provincial Hospital, Fuzhou 350001, China.
Jiang G; Shengli Clinical Medical College, Fujian Medical University, Fuzhou 350001, China; Department of Oncology, Fujian Provincial Hospital, Fuzhou 350001, China.
Lin X; Shengli Clinical Medical College, Fujian Medical University, Fuzhou 350001, China; Department of Thoracic Surgery, Fujian Provincial Hospital, Fuzhou 350001, China. Electronic address: .
Źródło:
Gene [Gene] 2023 Jan 30; Vol. 851, pp. 147053. Date of Electronic Publication: 2022 Nov 14.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Original Publication: Amsterdam, Elsevier/North-Holland, 1976-
MeSH Terms:
Fanconi Anemia*
Adenocarcinoma of Lung*/genetics
Lung Neoplasms*/genetics
Humans ; Macrophages ; Fanconi Anemia Complementation Group Proteins/genetics
Contributed Indexing:
Keywords: FANCI; LUAD; M1 macrophage; Prognostic
Substance Nomenclature:
0 (FANCI protein, human)
0 (Fanconi Anemia Complementation Group Proteins)
SCR Disease Name:
Fanconi Anemia, Complementation Group I
Entry Date(s):
Date Created: 20221117 Date Completed: 20221129 Latest Revision: 20221129
Update Code:
20240104
DOI:
10.1016/j.gene.2022.147053
PMID:
36395972
Czasopismo naukowe
FANCI, a member of the Fanconi anemia (FA) complementation group, normally associates with FANCD2 to play an important role in ribosome biogenesis and DNA repair. However, the correlation of FANCI with prognostic value and the molecular mechanism in patients with lung adenocarcinoma (LUAD) remains unclear. In the present study, bioinformatics analysis was performed on LUAD data from TCGA and GEO databases, and further confirmed by in vitro experiments. We found that a high level of FANCI was significantly correlated with a worse survival probability in patients with LUAD. Moreover, the results from in vitro experiments revealed high levels of FANCI in LUAD specimens and cell lines. Knockdown of FANCI expression in A549 and H460 cells significantly inhibited cell viability and clone formation of LUAD cells in vitro and in vivo. Furthermore, high FANCI levels were negatively correlated with a variety of tumor-infiltrating immune cells. Importantly, the overexpression of FANCI significantly inhibited the activation of M1 macrophages. All the data demonstrated that FANCI was a useful prognostic biomarker in patients with LUAD, and knockdown of FANCI inhibited tumor growth of LUAD cells in vitro and in vivo, partly by suppressing the activation of M1 macrophages.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2022. Published by Elsevier B.V.)

Ta witryna wykorzystuje pliki cookies do przechowywania informacji na Twoim komputerze. Pliki cookies stosujemy w celu świadczenia usług na najwyższym poziomie, w tym w sposób dostosowany do indywidualnych potrzeb. Korzystanie z witryny bez zmiany ustawień dotyczących cookies oznacza, że będą one zamieszczane w Twoim komputerze. W każdym momencie możesz dokonać zmiany ustawień dotyczących cookies