Evidence map›Paper›PMID 31501521›Full record

ArticleOncogene2020

Targeting the TR4 nuclear receptor-mediated lncTASR/AXL signaling with tretinoin increases the sunitinib sensitivity to better suppress the RCC progression.

Hangchuan Shi, Yin Sun, Miao He, Xiong Yang, Michiaki Hamada, Tsukasa Fukunaga, Xiaoping Zhang, Chawnshang Chang

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  9. AXL in cancer: a modulator of drug resistance and therapeutic target.Journal of experimental & clinical cancer research : CR · 2023
    Review
  10. Article
  11. Web Services for RNA-RNA Interaction Prediction.Methods in molecular biology (Clifton, N.J.) · 2023
    Review
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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 6 institutions in 4 countries.

Hangchuan Shi *Department of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Yin Sun *Radiation Oncology, The Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, NY, 14642, USA.
Miao HeRadiation Oncology, The Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, NY, 14642, USA.
Xiong YangDepartment of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Michiaki HamadaFaculty of Science and Engineering, Waseda University, Tokyo, 169-8555, Japan.
Tsukasa FukunagaFaculty of Science and Engineering, Waseda University, Tokyo, 169-8555, Japan.
Xiaoping ZhangDepartment of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. xzhang@hust.edu.cn.
Chawnshang ChangRadiation Oncology, The Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, NY, 14642, USA. chang@urmc.rochester.edu.
University of Rochester Medical Center · USChina Medical University · TWHuazhong University of Science and Technology · CNNational Institute of Advanced Industrial Science and Technology · JPUnion Hospital · CNWaseda University · JP

Funding

Stromal AR Roles in Prostate Hyperplasia and CancerR01CA156700 · NCI · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG, YEH, SHUYUAN · 2011 to 2015
$1.6M
NCI NIH HHS R01 CA156700
6 · The paper itself

Abstract

Renal cell carcinoma (RCC) is one of the most lethal urological tumors. Using sunitinib to improve the survival has become the first-line therapy for metastatic RCC patients. However, the occurrence of sunitinib resistance in the clinical application has curtailed its efficacy. Here we found TR4 nuclear receptor might alter the sunitinib resistance to RCC via altering the TR4/lncTASR/AXL signaling. Mechanism dissection revealed that TR4 could modulate lncTASR (ENST00000600671.1) expression via transcriptional regulation, which might then increase AXL protein expression via enhancing the stability of AXL mRNA to increase the sunitinib resistance in RCC. Human clinical surveys also linked the expression of TR4, lncTASR, and AXL to the RCC survival, and results from multiple RCC cell lines revealed that targeting this newly identified TR4-mediated signaling with small molecules, including tretinoin, metformin, or TR4-shRNAs, all led to increase the sunitinib sensitivity to better suppress the RCC progression, and our preclinical study using the in vivo mouse model further proved tretinoin had a better synergistic effect to increase sunitinib sensitivity to suppress RCC progression. Future successful clinical trials may help in the development of a novel therapy to better suppress the RCC progression.

Indexed as

AnimalsAntineoplastic Combined Chemotherapy ProtocolsAxl Receptor Tyrosine KinaseCarcinoma, Renal CellCell HypoxiaCell Line, TumorCell MovementDisease ProgressionDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansKidney NeoplasmsMetforminMiceProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesAxl Receptor Tyrosine KinaseMetforminNR2C2 protein, humanProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesReceptors, SteroidReceptors, Thyroid HormoneRNA, Long NoncodingRNA, Small InterferingSunitinibTretinoin

Identifiers

PMID31501521
PMCPMC6962095
OpenAlexW2973180611

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.