LINC00629 protects osteosarcoma cell from ER stress-induced apoptosis and facilitates tumour progression by elevating KLF4 stability

Escaping from ER stress-induced apoptosis plays an important role in the progression of many tumours. However, its molecular mechanism in osteosarcoma remains incompletely understood. The molecular mechanism was investigated using RNA sequencing, qRT-PCR and Western blot assays. The relationship bet...

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Published in:Journal of experimental & clinical cancer research 2022-12, Vol.41 (1), p.354-354, Article 354
Main Authors: Wang, Yuan, Zheng, Shuo, Han, Jian, Li, Na, Ji, Renchen, Li, Xiaodong, Han, Chuanchun, Zhao, Wenzhi, Zhang, Lu
Format: Article
Language:English
Subjects:
Analysis
Antisense RNA
Apoptosis
Apoptosis - genetics
B cells
Bone Neoplasms - pathology
Cell Line, Tumor
Cell Movement - genetics
Cell Proliferation
Chromatin
Gene Expression Regulation, Neoplastic
Genetic transcription
Humans
KLF4
LAMA4
Laminin
LINC00629
Luciferase
Metastasis
MicroRNAs - genetics
Osteosarcoma
Osteosarcoma - pathology
RNA sequencing
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
Ubiquitin
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Summary:Escaping from ER stress-induced apoptosis plays an important role in the progression of many tumours. However, its molecular mechanism in osteosarcoma remains incompletely understood. The molecular mechanism was investigated using RNA sequencing, qRT-PCR and Western blot assays. The relationship between LINC00629 and KLF4 was investigated using RNA pulldown and ubiquitylation assays. The transcriptional regulation of laminin subunit alpha 4 (LAMA4) by KLF4 was identified using bioinformatic analysis, a luciferase assay, and a chromatin immunoprecipitation assay. Here, we demonstrated that LINC00629 was increased under ER stress treatment. Elevated LINC00629 inhibited ER stress-induced osteosarcoma cell apoptosis and promoted clonogenicity and migration in vitro and in vivo. Further mechanistic studies indicated that LINC00629 interacted with KLF4 and suppressed its degradation, which led to a KLF4 increase in osteosarcoma. In addition, we also found that KLF4 upregulated LAMA4 expression by directly binding to its promoter and that LINC00629 inhibited ER stress-induced apoptosis and facilitated osteosarcoma cell clonogenicity and metastasis by activating the KLF4-LAMA4 pathway. Collectively, our data indicate that LINC00629 is a critical long noncoding RNA (lncRNA) induced by ER stress and plays an oncogenic role in osteosarcoma cell by activating the KLF4-LAMA4 axis.
ISSN:1756-9966
0392-9078
1756-9966
DOI:10.1186/s13046-022-02569-x