Evidence map›Paper›PMID 27754745›Full record

ArticleAutophagy2017

GFRA1 promotes cisplatin-induced chemoresistance in osteosarcoma by inducing autophagy.

Mihwa Kim, Ji-Yeon Jung, Seungho Choi, Hyunseung Lee, Liza D Morales, Jeong-Tae Koh, Sun Hun Kim, Yoo-Duk Choi, Chan Choi, Thomas J Slaga and 2 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Autophagy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed
9.3field-weighted citation impact, top 2% 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

102 citing papers in PubMed, 166 citations in OpenAlex.

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  18. Autophagy Regulators in Cancer.International journal of molecular sciences · 2023
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42 more citing papers are in PubMed but not listed here.

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

12 authors at 3 institutions in 2 countries.

Mihwa Kima Department of Oral Physiology , School of Dentistry, Chonnam National University , Gwangju , Korea.
Ji-Yeon Junga Department of Oral Physiology , School of Dentistry, Chonnam National University , Gwangju , Korea.
Seungho Choia Department of Oral Physiology , School of Dentistry, Chonnam National University , Gwangju , Korea.
Hyunseung Leeb Edinburg Regional Academic Health Center, Medical Research Division, University of Texas Health Science Center at San Antonio , Edinburg , TX , USA.
Liza D Moralesb Edinburg Regional Academic Health Center, Medical Research Division, University of Texas Health Science Center at San Antonio , Edinburg , TX , USA.
Jeong-Tae Kohd Dental Science Research Institute , Medical Research Center for Biomineralization Disorders, School of Dentistry, Chonnam National University , Gwangju , Korea.
Sun Hun Kimd Dental Science Research Institute , Medical Research Center for Biomineralization Disorders, School of Dentistry, Chonnam National University , Gwangju , Korea.
Yoo-Duk Choig Department of Pathology , Chonnam National University Medical School , Gwangju , Korea.
Chan Choig Department of Pathology , Chonnam National University Medical School , Gwangju , Korea.
Thomas J Slagac Department of Pharmacology , University of Texas Health Science Center at San Antonio , San Antonio , TX , USA.
Won Jae Kima Department of Oral Physiology , School of Dentistry, Chonnam National University , Gwangju , Korea.
Dae Joon Kimb Edinburg Regional Academic Health Center, Medical Research Division, University of Texas Health Science Center at San Antonio , Edinburg , TX , USA.
Chonnam National University · KRThe University of Texas Health Science Center at San Antonio · USChonnam National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent progress in chemotherapy has significantly increased its efficacy, yet the development of chemoresistance remains a major drawback. In this study, we show that GFRA1/GFRα1 (GDNF family receptor α 1), contributes to cisplatin-induced chemoresistance by regulating autophagy in osteosarcoma. We demonstrate that cisplatin treatment induced GFRA1 expression in human osteosarcoma cells. Induction of GFRA1 expression reduced cisplatin-induced apoptotic cell death and it significantly increased osteosarcoma cell survival via autophagy. GFRA1 regulates AMPK-dependent autophagy by promoting SRC phosphorylation independent of proto-oncogene RET kinase. Cisplatin-resistant osteosarcoma cells showed NFKB1/NFκB-mediated GFRA1 expression. GFRA1 expression promoted tumor formation and growth in mouse xenograft models and inhibition of autophagy in a GFRA1-expressing xenograft mouse model during cisplatin treatment effectively reduced tumor growth and increased survival. In cisplatin-treated patients, treatment period and metastatic status were associated with GFRA1-mediated autophagy. These findings suggest that GFRA1-mediated autophagy is a promising novel target for overcoming cisplatin resistance in osteosarcoma.

Indexed as

AutophagyDrug Resistance, NeoplasmAMP-Activated Protein KinasesAnimalsApoptosisBone NeoplasmsCell Line, TumorCell MovementCell ProliferationCell SurvivalCisplatinGlial Cell Line-Derived Neurotrophic Factor ReceptorsHEK293 CellsHumansMiceMice, NudeAMP-Activated Protein KinasesCisplatinGFRA1 protein, humanGfra1 protein, mouseGlial Cell Line-Derived Neurotrophic Factor ReceptorsMAS1 protein, humanProto-Oncogene MasRNA, Small InterferingAMPKautophagychemoresistanceGFRA1osteosarcomaSRC

Identifiers

PMID27754745
PMCPMC5240831
OpenAlexW2534236232

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.