Inhibition of lncRNA LINC00461/miR-216a/aquaporin 4 pathway suppresses cell proliferation, migration, invasion, and chemoresistance in glioma

Abstract: Long noncoding RNA (lncRNA) LINC00461 (LINC00461) is reported to be related to glioma progression. However, the mechanism of LINC00461 in glioma remains unclear. Expression of LINC00461, miRNA (miR)-216a, and aquaporin 4 (AQP4) was detected using real-time quantitative PCR (RT-qPCR) and western blotting. Proliferation, temozolomide (TMZ) resistance, migration, and invasion were assessed by MTT, colony formation, and transwell assays, respectively. The target binding among miR-216a, LINC00461, and AQP4 was confirmed by the luciferase reporter assay. The tumor growth was monitored in the xenograft experiment. LINC00461 was upregulated, and miR-216a was downregulated in glioma tissues and cells, and LINC00461 upregulation was correlated with large tumor size, higher WHO grade and recurrence, and poor overall survival. LINC00461 knockdown suppressed cell viability, abilities of cell cloning and migration and invasion, and TMZ resistance in glioma. Mechanically, LINC00461 was confirmed to sponge miR-216a to affect AQP4 expression. Rescue assays verified that miR-216a downregulation or AQP4 upregulation abrogated the inhibitory effect of LINC00461 knockdown on cell proliferation, migration, invasion, and TMZ resistance in vitro. Moreover, LINC00461 downregulation blocked the glioma tumor growth in vivo. In conclusion, LINC00461 knockdown inhibits glioma cell proliferation, migration, invasion, and TMZ resistance through miR-216a/AQP4 axis, suggesting LINC00461 as an oncogene in glioma progression.

Standort
Deutsche Nationalbibliothek Frankfurt am Main
Umfang
Online-Ressource
Sprache
Englisch

Erschienen in
Inhibition of lncRNA LINC00461/miR-216a/aquaporin 4 pathway suppresses cell proliferation, migration, invasion, and chemoresistance in glioma ; volume:15 ; number:1 ; year:2020 ; pages:532-543 ; extent:12
Open life sciences ; 15, Heft 1 (2020), 532-543 (gesamt 12)

Urheber
Peng, Yanguo
Wu, Wangchun
Shang, Zhanfang
Li, Wei
Chen, Shuiyu

DOI
10.1515/biol-2020-0048
URN
urn:nbn:de:101:1-2409201659498.140310754297
Rechteinformation
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
Letzte Aktualisierung
15.08.2025, 07:26 MESZ

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Beteiligte

  • Peng, Yanguo
  • Wu, Wangchun
  • Shang, Zhanfang
  • Li, Wei
  • Chen, Shuiyu

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