ArticleJournal of orthopaedic surgery and research2023
LINC00313 promotes the proliferation and inhibits the apoptosis of chondrocytes via regulating miR-525-5p/GDF5 axis.
Article in Journal of orthopaedic surgery and research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Article
- LINC00313 promotes the aggressiveness and tumorigenesis of cholangiocarcinoma through targeting miR-320b and MITF.Discover oncology · 2025Article
- Injectable self-assembled GDF5-containing dipeptide hydrogels for enhanced tendon repair.Materials today. Bio · 2024Article
- TGFβ-induced long non-coding RNA LINC00313 activates Wnt signaling and promotes cholangiocarcinoma.EMBO reports · 2024Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe present study aimed to explore the potentials of lncRNA LINC00313 in osteoarthritis (OA).
methodsqRT-PCR was performed to detect the expression of LINC00313 in OA tissues and cells. CCK-8 and EDU were used to detect cell proliferation. The ELISA test kit was conducted to detect the expression of inflammatory factors. Flow cytometry was used to detect the apoptosis rates. Western blot was applied to measure the protein expression. The luciferase reporter gene test was carried out to verify the relationship between miR-525-5p and LINC00313 or GDF5.
resultsThe data showed that the expression of LINC00313 was significantly down-regulated in OA tissues and cells. Functionally, LINC00313 promoted the proliferation of chondrocytes and suppressed the secretion of inflammatory factors and cell apoptosis. Moreover, LINC00313 functioned as a ceRNA to up-regulate the expression of GDF5 via sponging miR-525-5p. Luciferase and RNA pull-down assays further verified the interaction between miR-525-5p and LINC00313 (or GDF5). Moreover, overexpression of miR-525-5p or down-regulated GDF5 degraded the cellular functions of chondrocyte. Rescue experiments showed that the overexpression of miR-525-5p reversed the increase in cell viability and the decrease in pro-inflammatory factors and apoptosis rate mediated by LINC00313. The knockdown of GDF5 reversed the promotion of miR-525-5p knockdown on cell viability and the inhibition of pro-inflammatory factors and apoptosis rate.
conclusionsLINC00313 inhibited the development of OA through regulating miR-525-5p/GDF5 axis. LncRNA LINC00313 can be used as a potential target for the treatment of OA.
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Registered trials
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