Evidence map›Paper›PMID 24608861›Full record

ArticleCell cycle (Georgetown, Tex.)2014

E2F1 impairs all-trans retinoic acid-induced osteogenic differentiation of osteosarcoma via promoting ubiquitination-mediated degradation of RARα.

Lei Zhang, Qian Zhou, Ning Zhang, Weixu Li, Meidan Ying, Wanjing Ding, Bo Yang, Qiaojun He

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

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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

8 authors at 3 institutions in 2 countries.

Lei ZhangZhejiang Province Key Laboratory of Anti-Cancer Drug Research; College of Pharmaceutical Sciences; Zhejiang University; Hangzhou, China.
Qian ZhouZhejiang Province Key Laboratory of Anti-Cancer Drug Research; College of Pharmaceutical Sciences; Zhejiang University; Hangzhou, China.
Ning ZhangDepartment of Orthopedics; The Second Affiliated Hospital of Zhejiang University; Zhejiang University; Hangzhou, China.
Weixu LiDepartment of Orthopedics; The Second Affiliated Hospital of Zhejiang University; Zhejiang University; Hangzhou, China.
Meidan YingZhejiang Province Key Laboratory of Anti-Cancer Drug Research; College of Pharmaceutical Sciences; Zhejiang University; Hangzhou, China.
Wanjing DingZhejiang Province Key Laboratory of Anti-Cancer Drug Research; College of Pharmaceutical Sciences; Zhejiang University; Hangzhou, China.
Bo YangZhejiang Province Key Laboratory of Anti-Cancer Drug Research; College of Pharmaceutical Sciences; Zhejiang University; Hangzhou, China.
Qiaojun HeZhejiang Province Key Laboratory of Anti-Cancer Drug Research; College of Pharmaceutical Sciences; Zhejiang University; Hangzhou, China.
Pharmaceutical Biotechnology (Czechia) · CZSecond Affiliated Hospital of Zhejiang University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

All-trans retinoic acid (ATRA) is a widely used differentiation drug that can effectively induce osteogenic differentiation of osteosarcoma cells, but the underlying mechanism remains elusive, which limits the clinical application for ATRA in osteosarcoma patients. In this study, we identified E2F1 as a novel regulator involved in ATRA-induced osteogenic differentiation of osteosarcoma cells. We observed that osteosarcoma cells are coupled with individual differences in the expression levels of E2F1 in patients, and E2F1 impairs ATRA-induced differentiation of osteosarcoma cells. Moreover, remarkable anti-proliferative and differentiation-inducing effects of ATRA treatment are only observed in E2F1 low to negative expressed primary osteosarcoma cultures. These results strongly suggested that E2F1 may serve as a potent indicator for the effectiveness of ATRA treatment in osteosarcoma. Interestingly, E2F1 is found to downregulate retinoic acid receptor α (RARα), a key factor determines the effectiveness of ATRA. E2F1 specifically binds to RARα and promotes its ubiquitination-mediated degradation; as a consequence, RARα-mediated differentiation is inhibited in osteosarcoma. Therefore, our studies present E2F1 as a potent biomarker, as well as a therapeutic target for ATRA-based differentiation therapeutics, and raise the hope of using differentiation-based approaches for osteosarcoma patients.

Indexed as

UbiquitinationAntineoplastic AgentsBiomarkers, TumorCell Line, TumorE2F1 Transcription FactorHumansOsteogenesisOsteosarcomaProteolysisReceptors, Retinoic AcidRetinoic Acid Receptor alphaTretinoinAntineoplastic AgentsBiomarkers, TumorE2F1 protein, humanE2F1 Transcription FactorRARA protein, humanReceptors, Retinoic AcidRetinoic Acid Receptor alphaTretinoinall-trans retinoic acidATRAE2F1osteogenic differentiationosteosarcomaRARα

Identifiers

PMID24608861
PMCPMC4049964
OpenAlexW2062603666

What OpenQuestion holds

Textmetadata
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.