Evidence map›Paper›PMID 34933640›Full record

ArticleBioengineered2021

MYC-mediated miR-320a affects receptor activator of nuclear factor κB ligand (RANKL)-induced osteoclast formation by regulating phosphatase and tensin homolog (PTEN).

Hao Chen, Shaoshuo Li, Heng Yin, Zhen Hua, Yang Shao, Jie Wei, Jianwei Wang

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Polygonatum sibiricum component liquiritigenin restrains breast cancer cell invasion and migration by inhibiting HSP90 and chaperone-mediated autophagy.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024
    Article
  5. PTEN: an emerging target in rheumatoid arthritis?Cell communication and signaling : CCS · 2024
    Review
  6. Article
  7. Review
  8. Article
  9. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Hao ChenTraditional Chinese Medicine Orthopedics, Nanjing University of Chinese Medicine, Nanjing, JiangSu, China.
Shaoshuo LiTraditional Chinese Medicine Orthopedics, Nanjing University of Chinese Medicine, Nanjing, JiangSu, China.
Heng YinDepartment of Orthopedics and Traumatology, Wuxi Affiliated Hospital of Nanjing University of Chinese Medicine, Wuxi Hospital of Traditional Chinese Medicine, Wuxi, Jiangsu,China.
Zhen HuaDepartment of Orthopedics and Traumatology, Wuxi Affiliated Hospital of Nanjing University of Chinese Medicine, Wuxi Hospital of Traditional Chinese Medicine, Wuxi, Jiangsu,China.
Yang ShaoDepartment of Orthopedics and Traumatology, Wuxi Affiliated Hospital of Nanjing University of Chinese Medicine, Wuxi Hospital of Traditional Chinese Medicine, Wuxi, Jiangsu,China.
Jie WeiPICU, Yancheng Children's Hospital, Yancheng, Jiangsu, China.
Jianwei WangDepartment of Orthopedics and Traumatology, Wuxi Affiliated Hospital of Nanjing University of Chinese Medicine, Wuxi Hospital of Traditional Chinese Medicine, Wuxi, Jiangsu,China.
Nanjing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoporosis is a serious bone metabolism disease. Recent studies have shown that MYC could promote the formation of osteoclasts. Evidence has also shown that miR-320a could injure osteoblasts by inducing oxidative stress. By querying the database, we found that MYC has the potential to target and affect the expression of miR-320a. However, the effects of MYC and miR-320a on the the receptor activator of nuclear factor κB ligand (RANKL)-induced osteoclasts are unclear. In this study, we examined the relationship between MYC and miR-320a with luciferase reporter assay. To investigate the role of MYC and miR320a in osteoporosis, MYC or miR-320a expression were knocked down in RAW 264.7 cells. Meanwhile, the expression of markers of osteoclasts was detected with Western blotting. Finally, we inhibited the expression of PTEN in RAW 264.7 cells with miR-320a depletion and detected the expression of abovementioned proteins. MYC promoted the expression of miR-320a in RAW 264.7 cells by binding to the promoter of miR-320a. Inhibition of MYC and miR-320a suppressed the formation of RANKL-induced osteoclasts by inhibiting the expression of c-Fos, NFATc1, TRAP and CTSK. Moreover, the expression of c-Fos, NFATc1, TRAP and CTSK was rescued and the RANKL-induced osteoclasts was promoted after the repressing the expression of PTEN. In conclusion, MYC enhanced the formation of RANKL-induced osteoclasts by modulating the miR-320a/PTEN pathway.

Indexed as

AnimalsBase SequenceMiceMicroRNAsOsteoclastsProto-Oncogene Proteins c-mycPTEN PhosphohydrolaseRANK LigandRAW 264.7 CellsUp-RegulationMicroRNAsMirn320 microRNA, mouseProto-Oncogene Proteins c-mycPTEN PhosphohydrolaseRANK LigandmiR-320aMYCosteoclastsPTEN

Identifiers

PMID34933640
PMCPMC8810188
OpenAlexW4200112318

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.