Long non-coding ROR promotes the progression of papillary thyroid carcinoma through regulation of the TESC/ALDH1A1/TUBB3/PTEN axis.
Aldehyde Dehydrogenase 1 Family
/ genetics
Animals
Calcium-Binding Proteins
/ genetics
Cell Line, Tumor
Cell Movement
/ genetics
Cell Proliferation
/ genetics
Gene Expression Regulation, Neoplastic
/ genetics
Humans
Mice
Mice, Nude
PTEN Phosphohydrolase
/ genetics
RNA, Long Noncoding
/ genetics
Retinal Dehydrogenase
/ genetics
Thyroid Cancer, Papillary
/ metabolism
Thyroid Neoplasms
/ metabolism
Tubulin
/ genetics
Journal
Cell death & disease
ISSN: 2041-4889
Titre abrégé: Cell Death Dis
Pays: England
ID NLM: 101524092
Informations de publication
Date de publication:
16 02 2022
16 02 2022
Historique:
received:
13
04
2021
accepted:
21
09
2021
revised:
02
09
2021
entrez:
17
2
2022
pubmed:
18
2
2022
medline:
9
4
2022
Statut:
epublish
Résumé
Papillary thyroidal carcinoma (PTC) is a common endocrine cancer that plagues people across the world. The potential roles of long non-coding RNAs (lncRNAs) in PTC have gained increasing attention. In this study, we aimed to explore whether lncRNA ROR affects the progression of PTC, with the involvement of tescalcin (TESC)/aldehyde dehydrogenase isoform 1A1 (ALDH1A1)/βIII-tubulin (TUBB3)/tensin homolog (PTEN) axis. PTC tumor and adjacent tissues were obtained, followed by measurement of lncRNA ROR and TESC, ALDH1A1, and TUBB3 expression. Interactions among lncRNA ROR, TESC, ALDH1A1, TUBB3, and PTEN were evaluated by ChIP assay, RT-qPCR, or western blot analysis. After ectopic expression and depletion experiments in PTC cells, MTT and colony formation assay, Transwell assay, and flow cytometry were performed to detect cell viability and colony formation, cell migration and invasion, and apoptosis, respectively. In addition, xenograft in nude mice was performed to test the effects of lncRNA ROR and PTEN on tumor growth in PTC in vivo. LncRNA ROR, TESC, ALDH1A1, and TUBB3 were highly expressed in PTC tissues and cells. Overexpression of lncRNA ROR activated TESC by inhibiting the G9a recruitment on the promoter of TESC and histone H3-lysine 9me methylation. Moreover, TESC upregulated ALDH1A1 expression to increase TUBB3 expression, which then reduced PTEN expression. Overexpression of lncRNA ROR, TESC, ALDH1A1 or TUBB3 and silencing of PTEN promoted PTC cell viability, colony formation, migration, and invasion while suppressing apoptosis. Moreover, overexpression of lncRNA ROR increased tumor growth by inhibiting PTEN in vivo. Taken together, the current study demonstrated that lncRNA ROR mediated TESC/ALDH1A1/TUBB3/PTEN axis, thereby facilitating the development of PTC.
Identifiants
pubmed: 35173149
doi: 10.1038/s41419-021-04210-9
pii: 10.1038/s41419-021-04210-9
pmc: PMC8850450
doi:
Substances chimiques
Calcium-Binding Proteins
0
Linc-RNA-RoR, human
0
RNA, Long Noncoding
0
TESC protein, human
0
TUBB3 protein, human
0
Tubulin
0
Aldehyde Dehydrogenase 1 Family
EC 1.2.1
ALDH1A1 protein, human
EC 1.2.1.36
Retinal Dehydrogenase
EC 1.2.1.36
PTEN Phosphohydrolase
EC 3.1.3.67
PTEN protein, human
EC 3.1.3.67
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
157Informations de copyright
© 2022. The Author(s).
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