Evidence map›Paper›PMID 26797758›Full record

ArticleOncotarget2016

Crosstalk between ATF4 and MTA1/HDAC1 promotes osteosarcoma progression.

Heng Zeng, Jin-Ming Zhang, Yu Du, Jiang Wang, Ye Ren, Mi Li, Hao Li, Zhuo Cai, Qian Chu, Caihong Yang

RetractedOpen access · diamondAbstract readRetracted Publication
In one paragraph

Article in Oncotarget, 2016. 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 It has been retracted, and should not be counted.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 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Osteosarcoma and Metastasis.Frontiers in oncology · 2021
    Review
  13. Article
  14. Review
  15. Article
  16. Oncogenic role of SFRP2 in p53-mutant osteosarcoma development via autocrine and paracrine mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Heng ZengDepartment of Orthopedics, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Jin-Ming ZhangDepartment of Orthopedics, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Yu DuDepartment of Orthopedics, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Jiang WangDepartment of Orthopedics, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Ye RenDepartment of Orthopedics, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Mi LiDepartment of Orthopedics, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Hao LiDepartment of Orthopedics, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Zhuo CaiDepartment of Orthopedics, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Qian ChuDepartment of Oncology, Tongji Hospital of Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Caihong YangDepartment of Orthopedics, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Huazhong University of Science and Technology · CNTongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The stress response gene activating transcription factor 4 (ATF4) is involved in metastatic behavior and cellular protection. Here we show that ATF4 is upregulated in osteosarcoma (OS) cell lines and patient clinical samples as compared to matched non-tumor tissue. Overexpression of ATF4 in OS cells promoted cell proliferation, migration and lung metastasis. Furthermore, the expression of ATF4 was markedly reduced in metastasis associated protein (MTA1) or histone deacetylase 1 (HDAC1) knockdown OS cells, but MTA1 overexpression increased the stability and activity of ATF4 protein via ATF4 deacetylation by HDAC1. ATF4 in turn enhanced the expression of MTA1 and HDAC1 at the transcription level, suggesting a positive feedback loop between ATF4 and MTA1/HDAC1. Clinically, the level of ATF4 was positively correlated with that of MTA1 in OS. Mice injected with ATF4-overexpressing cells exhibited a higher rate of tumor growth, and the average weight of these tumors was ~90% greater than the controls. Taken together, these data establish a direct correlation between ATF4-induced OS progression and MTA1/HDAC1-associated metastasis, and support the potential therapeutic value of targeting ATF4 in the treatment of OS.

Indexed as

Activating Transcription Factor 4AnimalsApoptosisBlotting, WesternBone NeoplasmsCell MovementCell ProliferationChromatin ImmunoprecipitationDisease ProgressionFollow-Up StudiesHistone Deacetylase 1Histone DeacetylasesHumansImmunoenzyme TechniquesImmunoprecipitationLung NeoplasmsActivating Transcription Factor 4ATF4 protein, humanHDAC1 protein, humanHistone Deacetylase 1Histone DeacetylasesMTA1 protein, humanRepressor ProteinsRNA, MessengerTrans-Activatorsactivating transcription factor 4histone deacetylase 1metastasis-associated protein 1osteosarcoma

Identifiers

PMID26797758
PMCPMC4872789
OpenAlexW2334198080

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.