Evidence map›Paper›PMID 26973243›Full record

ArticleOncogene2016

Differential regulation of LncRNA-SARCC suppresses VHL-mutant RCC cell proliferation yet promotes VHL-normal RCC cell proliferation via modulating androgen receptor/HIF-2α/C-MYC axis under hypoxia.

W Zhai, Y Sun, M Jiang, M Wang, T A Gasiewicz, J Zheng, C Chang

Open access · bronzeAbstract read
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In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% 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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.

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  15. Noncoding RNAs as sensors of tumor microenvironmental stress.Journal of experimental & clinical cancer research : CR · 2022
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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

7 authors at 4 institutions in 3 countries.

W ZhaiDepartment of Urology, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China.
Y SunGeorge Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and the Wilmot Cancer Center, University of Rochester Medical Center, Rochester, NY, USA.
M JiangLab of Nuclear Receptors and Cancer Research, School of Medicine, Nantong University, Nantong, Jiangsu, China.
M WangGeorge Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and the Wilmot Cancer Center, University of Rochester Medical Center, Rochester, NY, USA.
T A GasiewiczDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, USA.
J ZhengDepartment of Urology, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China.
C ChangGeorge Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and the Wilmot Cancer Center, University of Rochester Medical Center, Rochester, NY, USA.
University of Rochester Medical Center · USTongji University · CNChina Medical University · TWNantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is well established that hypoxia contributes to tumor progression in a hypoxia inducible factor-2α (HIF-2α)-dependent manner in renal cell carcinoma (RCC), yet the role of long noncoding RNAs (LncRNAs) involved in hypoxia-mediated RCC progression remains unclear. Here we demonstrate that LncRNA-SARCC (Suppressing Androgen Receptor in Renal Cell Carcinoma) is differentially regulated by hypoxia in a von Hippel-Lindau (VHL)-dependent manner both in RCC cell culture and clinical specimens. LncRNA-SARCC can suppress hypoxic cell cycle progression in the VHL-mutant RCC cells while derepress it in the VHL-restored RCC cells. Mechanism dissection reveals that LncRNA-SARCC can post-transcriptionally regulate androgen receptor (AR) by physically binding and destablizing AR protein to suppress AR/HIF-2α/C-MYC signals. In return, HIF-2α can transcriptionally regulate the LncRNA-SARCC expression via binding to hypoxia-responsive elements on the promoter of LncRNA-SARCC. The negative feedback modulation between LncRNA-SARCC/AR complex and HIF-2α signaling may then lead to differentially modulated RCC progression in a VHL-dependent manner. Together, these results may provide us a new therapeutic approach via targeting this newly identified signal from LncRNA-SARCC to AR-mediated HIF-2α/C-MYC signals against RCC progression.

Indexed as

Basic Helix-Loop-Helix ProteinsCarcinoma, Renal CellCell Line, TumorCell ProliferationEndothelial PAS Domain-Containing Protein 1Gene Expression Regulation, NeoplasticHumansPromoter Regions, GeneticProto-Oncogene Proteins c-mycReceptors, AndrogenRNA, Long NoncodingSignal TransductionVon Hippel-Lindau Tumor Suppressor ProteinAR protein, humanBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1long noncoding SARCC, humanMYC protein, humanProto-Oncogene Proteins c-mycReceptors, AndrogenRNA, Long NoncodingVHL protein, humanVon Hippel-Lindau Tumor Suppressor Protein

Identifiers

PMID26973243
OpenAlexW2299015032

What OpenQuestion holds

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Registered trials

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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.