Evidence map›Paper›PMID 34012023›Full record

ArticleExperimental & molecular medicine2021

PAX8-AS1 knockdown facilitates cell growth and inactivates autophagy in osteoblasts via the miR-1252-5p/GNB1 axis in osteoporosis.

Caiqiang Huang, Runguang Li, Changsheng Yang, Rui Ding, Qingchu Li, Denghui Xie, Rongkai Zhang, Yiyan Qiu

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Experimental & molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
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  7. Autophagy: regulating the seesaw of bone-fat balance.Frontiers in cell and developmental biology · 2025
    Review
  8. Article
  9. Noncoding RNAs: the crucial role of programmed cell death in osteoporosis.Frontiers in cell and developmental biology · 2024
    Review
  10. Article
  11. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Caiqiang Huang *Division of Spine Surgery, Section II, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Southern Medical University, Academy of Orthopedics of Guangdong Province, Guangzhou, Guangdong, China.
Runguang Li *Division of Foot and Ankle Surgery, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Southern Medical University, Academy of Orthopedics of Guangdong Province, Guangzhou, Guangdong, China.ORCID http://orcid.org/0000-0002-4703-7180
Changsheng YangDivision of Spine Surgery, Section II, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Southern Medical University, Academy of Orthopedics of Guangdong Province, Guangzhou, Guangdong, China.
Rui DingDivision of Spine Surgery, Section II, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Southern Medical University, Academy of Orthopedics of Guangdong Province, Guangzhou, Guangdong, China.
Qingchu LiDivision of Spine Surgery, Section II, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Southern Medical University, Academy of Orthopedics of Guangdong Province, Guangzhou, Guangdong, China.
Denghui XieDivision of Joint Surgery, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Southern Medical University, Academy of Orthopedics of Guangdong Province, Guangzhou, Guangdong, China.
Rongkai ZhangDivision of Joint Surgery, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Southern Medical University, Academy of Orthopedics of Guangdong Province, Guangzhou, Guangdong, China.
Yiyan QiuDivision of Spine Surgery, Section II, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Southern Medical University, Academy of Orthopedics of Guangdong Province, Guangzhou, Guangdong, China. qiuyiy55@hotmail.com.
Third Affiliated Hospital of Southern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoporosis (OP) is the most common systematic bone disorder among elderly individuals worldwide. Long noncoding RNAs (lncRNAs) are involved in biological processes in various human diseases. It has been previously revealed that PAX8 antisense RNA 1 (PAX8-AS1) is upregulated in OP. However, its molecular mechanism in OP remains unclear. Therefore, we specifically designed this study to determine the specific role of PAX8-AS1 in OP. We first established a rat model of OP and then detected PAX8-AS1 expression in the rats with RT-qPCR. Next, to explore the biological function of PAX8-AS1 in osteoblasts, in vitro experiments, such as Cell Counting Kit-8 (CCK-8) assays, flow cytometry, western blotting and immunofluorescence (IF) staining, were conducted. Subsequently, we performed bioinformatic analysis and luciferase reporter assays to predict and identify the relationships between microRNA 1252-5p (miR-1252-5p) and both PAX8-AS1 and G protein subunit beta 1 (GNB1). Additionally, rescue assays in osteoblasts clarified the regulatory network of the PAX8-AS1/miR-1252-5p/GNB1 axis. Finally, in vivo loss-of-function studies verified the role of PAX8-AS1 in OP progression. The results illustrated that PAX8-AS1 was upregulated in the proximal tibia of OP rats. PAX8-AS1 silencing promoted the viability and inhibited the apoptosis and autophagy of osteoblasts. PAX8-AS1 interacted with miR-1252-5p. GNB1 was negatively regulated by miR-1252-5p. In addition, the impacts of PAX8-AS1 knockdown on osteoblasts were counteracted by GNB1 overexpression. PAX8-AS1 depletion suppressed OP progression by inhibiting apoptosis and autophagy in osteoblasts. In summary, PAX8-AS1 suppressed the viability and activated the autophagy of osteoblasts via the miR-1252-5p/GNB1 axis in OP.

Indexed as

AnimalsApoptosisAutophagyCell Line, TumorDisease Models, AnimalFemaleGene Knockdown TechniquesGene SilencingGTP-Binding Protein beta SubunitsMicroRNAsModels, BiologicalOsteoblastsOsteoporosisPAX8 Transcription FactorRatsRNA, AntisenseGTP-Binding Protein beta SubunitsMicroRNAsPAX8 Transcription FactorRNA, AntisenseRNA, Long Noncoding

Identifiers

PMID34012023
PMCPMC8178389
OpenAlexW3163671245

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.