Evidence map›Paper›PMID 35117781›Full record

ArticleTranslational cancer research2020

MicroRNA-494 represses osteosarcoma development by modulating ASK-1 related apoptosis complexes.

Gan Gao, Yuekui Jian

RetractedOpen access · diamondAbstract readRetracted Publication
In one paragraph

Article in Translational cancer research, 2020. 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 It has been retracted, and should not be counted.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 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 53% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Role of microRNA-494 in tumor progression.American journal of translational research · 2023
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Gan GaoGuizhou Provincial People's Hospital, Guiyang, China.
Yuekui JianGuizhou Provincial People's Hospital, Guiyang, China.
Guizhou Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicroRNA (miR)-494 had been proven to be involved in tumor pathogenesis, while studies on miR-494 and osteosarcoma (OS) are still limited. In the current study, we aimed to explore the expression pattern and the roles of miR-494 in the development of OS.

methodsMouse models and osteoblastic cells were used to investigate the functions of miR-494. A case-control study including 87 OS patients and 100 controls was also conducted to investigate the prognostic value of miR-494.

resultsAnimal researches and human studies showed that miR-494 expression level in OS tissue (OST) was down-regulated compared to paracancerous tissue (PT), and had a significant positive association with its level in serum (P<0.05). Gain of miR-494 function suppressed OS tumor growth and promoted apoptosis of OS cells, while loss of miR-494 inhibited apoptosis and promoted invasion of osteoblastic cells. MiR-494 expressions in both OST and serum were correlated with the T stage, lymph node metastasis and distant metastasis of OS (P<0.05). Results of survival analysis showed that compared to patients with high miR-494 level, the overall survival rate in 24 months was significantly lower in the low miR-494 group (P<0.05). In vitro study revealed that miR-494 interacted with apoptosis signal regulating kinase 1 (ASK-1)/serine-threonine kinase receptor-associated protein (STRAP)/14-3-3 complex to promote the activation of tumor necrosis factor-α (TNF-α)/ASK-1-mediated apoptosis.

conclusionsThese results revealed that miR-494 functioned as a tumor suppressor and improved the prognosis of OS via modulating apoptosis complexes.

Indexed as

apoptosisMicroRNA-494 (miR-494)osteosarcoma (OS)prognosis

Identifiers

PMID35117781
PMCPMC8798096
OpenAlexW3040731138

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.