LncRNA SNHG11 enhances bevacizumab resistance in colorectal cancer by mediating miR-1207-5p/ABCC1 axis.
Journal
Anti-cancer drugs
ISSN: 1473-5741
Titre abrégé: Anticancer Drugs
Pays: England
ID NLM: 9100823
Informations de publication
Date de publication:
01 07 2022
01 07 2022
Historique:
pubmed:
25
3
2022
medline:
20
5
2022
entrez:
24
3
2022
Statut:
ppublish
Résumé
Long noncoding RNAs (lncRNAs) have been reported to serve as vital regulators in the chemoresistance of human cancers, including colorectal cancer (CRC). In this study, we aimed to explore the functions of lncRNA small nucleolar RNA host gene 11 (SNHG11) in the resistance of CRC to bevacizumab. Quantitative real-time PCR, western blot assay or immunohistochemistry assay were performed to examine the expression of SNHG11, microRNA-1207-5p (miR-1207-5p), ATP binding cassette subfamily C member 1 (ABCC1) and Ki67. Cell Counting Kit-8 assay was conducted to evaluate bevacizumab resistance and cell viability. 5'-ethynyl-2'-deoxyuridine analysis, flow cytometry analysis and wound-healing assay were conducted for cell proliferation, apoptosis and migration, respectively. Dual-luciferase reporter assay and RNA immunoprecipitation assay were employed to analyze the relations among SNHG11, miR-1207-5p and ABCC1. Murine xenograft model assay was employed to analyze bevacizumab resistance in vivo. The exosomes were observed under transmission electron microscopy. SNHG11 was overexpressed in bevacizumab-resistant CRC tissues and cells. Knockdown of SNHG11 restrained bevacizumab resistance, repressed cell proliferation and migration, and promoted apoptosis in bevacizumab-resistant CRC cells. MiR-1207-5p served as the target of SNHG11 and SNHG11 regulated bevacizumab resistance by targeting miR-1207-5p. ABCC1 was the target gene of miR-1207-5p. Overexpression of miR-1207-5p inhibited bevacizumab resistance and cell progression in bevacizumab-resistant CRC cells, with ABCC1 elevation abrogated the impacts. SNHG11 silencing repressed bevacizumab resistance in vivo. In addition, exosomal SNHG11 was upregulated in bevacizumab-resistant CRC cells. SNHG11 contributes to bevacizumab resistance in CRC depending on the modulation of miR-1207-5p and ABCC1.
Identifiants
pubmed: 35324517
doi: 10.1097/CAD.0000000000001289
pii: 00001813-202207000-00007
doi:
Substances chimiques
MIRN1207 microRNA, human
0
MicroRNAs
0
RNA, Circular
0
RNA, Long Noncoding
0
Bevacizumab
2S9ZZM9Q9V
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
575-586Informations de copyright
Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.
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