Knockdown of lncRNA LINC00662 suppresses malignant behaviour of osteosarcoma cells via competition with miR-30b-3p to regulate ELK1 expression
© 2022. The Author(s)..
PURPOSE: Osteosarcoma is a type of bone malignancy that mainly occurred in teenagers. This investigation is aimed to clarify the effect of long non-coding RNA (lncRNA) LINC00662 on the proliferation, migration, and invasion in osteosarcoma and explore the underlying action mechanisms.
METHODS: The mRNA expression of LINC00662 was determined by real-time quantitative polymerase chain reaction. Cell proliferation, migration, and invasion were evaluated by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, wound healing, and transwell assays, respectively. A dual-luciferase reporter assay was used to validate the target relationships Between microRNA (miR)-30b-3p and LINC00662/ ETS domain-containing protein 1 (ELK1). Western blotting was performed to determine the protein expression of ELK1. Xenograft model was established to evaluate the effects of LINC00662 silencing on tumor growth in vivo.
RESULTS: LncRNA LINC00662 and ELK1 were significantly increased, while miR-30b-3p was reduced in osteosarcoma tissues. The results of functional experiments indicated that transfection of small hairpin (sh)-LINC00662 and miR-30b-3p mimics repressed the migration, invasion, and proliferation of osteosarcoma cells. LncRNA LINC00662 also appeared to sponge miR-30b-3p in order to affect the expression of ELK1. Simultaneously, there were weak negative correlations between the expression of miR-30b-3p and LINC00662/ELK1 in osteosarcoma tissues. Rescue experiments suggested that ELK1 overexpression and downregulation of miR-30b-3p reversed the suppressive effects of sh-LINC00662 on the cell migration, invasion, and proliferation in osteosarcoma.
CONCLUSIONS: The current study indicated that knockdown of LINC00662 repressed cell migration, invasion, and proliferation through sponging miR-30b-3p to regulate the expression of ELK1 in osteosarcoma. These results may uncover a promising target for the treatment of osteosarcoma.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2022 |
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| Erschienen: |
2022 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:17 |
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| Enthalten in: |
Journal of orthopaedic surgery and research - 17(2022), 1 vom: 05. Feb., Seite 74 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Wang, Bin [VerfasserIn] |
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| Links: |
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| Themen: |
ELK1 |
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| Anmerkungen: |
Date Completed 22.03.2022 Date Revised 22.03.2022 published: Electronic Citation Status MEDLINE |
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| doi: |
10.1186/s13018-022-02964-2 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM33656063X |
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| 035 | |a (NLM)35123530 | ||
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| 041 | |a eng | ||
| 100 | 1 | |a Wang, Bin |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Knockdown of lncRNA LINC00662 suppresses malignant behaviour of osteosarcoma cells via competition with miR-30b-3p to regulate ELK1 expression |
| 264 | 1 | |c 2022 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
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| 500 | |a Date Completed 22.03.2022 | ||
| 500 | |a Date Revised 22.03.2022 | ||
| 500 | |a published: Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © 2022. The Author(s). | ||
| 520 | |a PURPOSE: Osteosarcoma is a type of bone malignancy that mainly occurred in teenagers. This investigation is aimed to clarify the effect of long non-coding RNA (lncRNA) LINC00662 on the proliferation, migration, and invasion in osteosarcoma and explore the underlying action mechanisms | ||
| 520 | |a METHODS: The mRNA expression of LINC00662 was determined by real-time quantitative polymerase chain reaction. Cell proliferation, migration, and invasion were evaluated by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, wound healing, and transwell assays, respectively. A dual-luciferase reporter assay was used to validate the target relationships Between microRNA (miR)-30b-3p and LINC00662/ ETS domain-containing protein 1 (ELK1). Western blotting was performed to determine the protein expression of ELK1. Xenograft model was established to evaluate the effects of LINC00662 silencing on tumor growth in vivo | ||
| 520 | |a RESULTS: LncRNA LINC00662 and ELK1 were significantly increased, while miR-30b-3p was reduced in osteosarcoma tissues. The results of functional experiments indicated that transfection of small hairpin (sh)-LINC00662 and miR-30b-3p mimics repressed the migration, invasion, and proliferation of osteosarcoma cells. LncRNA LINC00662 also appeared to sponge miR-30b-3p in order to affect the expression of ELK1. Simultaneously, there were weak negative correlations between the expression of miR-30b-3p and LINC00662/ELK1 in osteosarcoma tissues. Rescue experiments suggested that ELK1 overexpression and downregulation of miR-30b-3p reversed the suppressive effects of sh-LINC00662 on the cell migration, invasion, and proliferation in osteosarcoma | ||
| 520 | |a CONCLUSIONS: The current study indicated that knockdown of LINC00662 repressed cell migration, invasion, and proliferation through sponging miR-30b-3p to regulate the expression of ELK1 in osteosarcoma. These results may uncover a promising target for the treatment of osteosarcoma | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a ELK1 | |
| 650 | 4 | |a Long non-coding RNA LINC00662 | |
| 650 | 4 | |a Osteosarcoma | |
| 650 | 4 | |a miR-30b-3p | |
| 650 | 4 | |a microRNAs | |
| 650 | 7 | |a ELK1 protein, human |2 NLM | |
| 650 | 7 | |a MIRN30b microRNA, human |2 NLM | |
| 650 | 7 | |a MicroRNAs |2 NLM | |
| 650 | 7 | |a RNA, Long Noncoding |2 NLM | |
| 650 | 7 | |a ets-Domain Protein Elk-1 |2 NLM | |
| 700 | 1 | |a Xu, Zhengfeng |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Xiuhui |e verfasserin |4 aut | |
| 700 | 1 | |a Xia, Shengli |e verfasserin |4 aut | |
| 700 | 1 | |a Cai, Pan |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Minghui |e verfasserin |4 aut | |
| 700 | 1 | |a Gao, Zhenchao |e verfasserin |4 aut | |
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| 773 | 1 | 8 | |g volume:17 |g year:2022 |g number:1 |g day:05 |g month:02 |g pages:74 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1186/s13018-022-02964-2 |3 Volltext |
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