Evidence map›Paper›PMID 24384722›Full record

ArticleCell death & disease2014

Gli1 inhibition suppressed cell growth and cell cycle progression and induced apoptosis as well as autophagy depending on ERK1/2 activity in human chondrosarcoma cells.

Y Sun, W Guo, T Ren, W Liang, W Zhou, Q Lu, G Jiao, T Yan

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 64 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 2 institutions in 1 country.

Y SunMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing, China.
W GuoMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing, China.
T RenMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing, China.
W LiangMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing, China.
W ZhouMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing, China.
Q LuMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing, China.
G JiaoMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing, China.
T YanMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing, China.
Peking University People's Hospital · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor glioma-associated oncogene 1 (Gli1) has been recognized as a very important nuclear executor at the distal end of the Hedgehog (Hh) signal pathway, which has crucial roles in regulating many developmental processes, such as pattern formation, differentiation, proliferation, and apoptosis. Overexpression of patched 1 protein and Gli1 or constitutively active Indian Hedgehog (IHh)-parathyroid hormone-related protein signal pathway may lead to musculoskeletal tumorigenesis. However, for chondrosarcoma few studies have paid close attention to the IHh-Gli1 signal transduction cascade and more work needs to be carried out to fully elucidate Gli1 protein functions. Here we show that the IHh signal pathway was activated in chondrosarcoma, and knocking down the expression of Gli1 attenuated the disturbed IHh signal pathway, which not only suppressed cell proliferation and promoted G2/M cell cycle arrest but also enhanced cell apoptosis by downregulating Bcl-2 and Bcl-xl expression. Furthermore, Gli1 downregulation, not cyclopamine, induced autophagy by regulating mTOR phosphorylation, and inhibition of autophagy prevented Gli1 small interfering RNA-mediated cell death. We also demonstrated that extracellular signal-regulated kinase 1/2 activity may mediate these antiproliferative events induced by Gli1 inhibition. These results indicate that Gli1 inhibition could ultimately provide a promising new approach for chondrosarcoma treatment.

Indexed as

ApoptosisAutophagyCell CycleCell ProliferationChondrosarcomaDown-RegulationHedgehog ProteinsHumansMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Neoplasms, Connective and Soft TissueSignal TransductionTranscription FactorsZinc Finger Protein GLI1GLI1 protein, humanHedgehog ProteinsIHH protein, humanMAPK1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Transcription FactorsZinc Finger Protein GLI1

Identifiers

PMID24384722
PMCPMC4040663
OpenAlexW2040308995

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.