Evidence map›Paper›PMID 29618948›Full record

ArticleCancer cell international2018

microRNA-338-3p inhibits proliferation, migration, invasion, and EMT in osteosarcoma cells by targeting activator of 90 kDa heat shock protein ATPase homolog 1.

Riliang Cao, Jianli Shao, Yabin Hu, Liang Wang, Zhizhong Li, Guodong Sun, Xiaoliang Gao

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
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  4. The role of Aha1 in cancer and neurodegeneration.Frontiers in molecular neuroscience · 2024
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 1 country.

Riliang Cao *Department of Pediatric Surgery, Guangdong Women and Children Hospital, Guangzhou, 511400, China.
Jianli Shao *Department of Orthopedic and Traumatology, First Affiliated Hospital, Jinan University, Guangzhou, 510632, China. tshaojianli@126.com.
Yabin Hu *Department of Spinal Surgery, The Sixth Affiliated Hospital of Xinjiang Medical University, Ürümqi, 830002, Xinjiang, China. hyb4499@126.com.
Liang WangDepartment of Oncology, First Affiliated Hospital, Jinan University, Guangzhou, 510632, China.
Zhizhong LiDepartment of Orthopedic and Traumatology, First Affiliated Hospital, Jinan University, Guangzhou, 510632, China.
Guodong SunDepartment of Orthopedic and Traumatology, First Affiliated Hospital, Jinan University, Guangzhou, 510632, China.
Xiaoliang GaoDepartment of Spinal Surgery, The Sixth Affiliated Hospital of Xinjiang Medical University, Ürümqi, 830002, Xinjiang, China.
First Affiliated Hospital of Jinan University · CNGuangdong Province Women and Children Hospital · CNSixth Affiliated Hospital of Xinjiang Medical University · CNXinjiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOsteosarcoma (OS) is a rare, malignant bone tumor that primarily affects adolescents and has a high degree of malignancy and high incidence of recurrence and metastasis. Our study aimed to explore the role of miR-338-3p in OS cells.

methodsqRT-qPCR was performed to quantify miR-338-3p expression levels in OS tissue samples and in three common OS cell lines. MG-63 and Saos2 cells were separately transfected with miR-338-3p or NC mimics and miR-338-3p expression levels was determined by qRT-PCR. Cell proliferation was monitored using the Cell Counting Kit-8. Flow cytometer analysis was carried out to determine the distribution of cell cycle stages and apoptosis. Transwell assay was performed to measure the migratory and invasive capacities of MG-63 and Saos2 cells. The expression of Vimentin and E-cadherin was detected by western blot. Luciferase reporter assay, qRT-PCR and western blotting were performed to confirm the target of miR-338-3p.

resultsAnalysis by qRT-PCR revealed that miR-338-3p was downregulated in the tissue samples of 20 OS patients when compared with that in their matched adjacent non-tumor tissues. Furthermore, miR-338-3p was significantly downregulated in three common OS cell lines, namely, MG-63, Saos2, and HOS, when compared with that in the human osteoblast cell line hFOB1.19. Analysis by luciferase reporter assay, qRT-PCR, and western blotting revealed that activator of 90 kDa heat shock protein ATPase homolog 1 (AHSA1) is a direct target of miR-338-3p. miR-338-3p overexpression led to significant reduction in AHSA1 protein levels in MG63 and Saos2 cells. miR-338-3p overexpression reduced cell viability and migration and invasion behavior of MG63 and Saos2 cells. In addition, miR-338-3p overexpression suppressed epithelial-mesenchymal transition (EMT), induced a significant G1-phase arrest and did not affect the apoptosis in both MG-63 and Saos2 cells. Moreover, overexpression of AHSA1 reversed the inhibitory effect of miR-338-3p overexpression on proliferation, cell cycle, apoptosis, EMT, migration, and invasion of MG63 and Saos2 cells, thereby suggesting that miR-338-3p acts as a tumor suppressor in OS cells by targeting AHSA1.

conclusionsmiR-338-3p/AHSA1 can serve as a potential therapeutic target for OS therapy.

Indexed as

Activator of 90 kDa heat shock protein ATPase homolog 1microRNA-338-3pOsteosarcomaTranslational repressionTumor suppressor

Identifiers

PMID29618948
PMCPMC5879792
OpenAlexW2807398426

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.