Evidence map›Paper›PMID 31131187›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2019

Tumor Cell "Slimming" Regulates Tumor Progression through PLCL1/UCP1-Mediated Lipid Browning.

Zhiyong Xiong, Wen Xiao, Lin Bao, Wei Xiong, Haibing Xiao, Yan Qu, Changfei Yuan, Hailong Ruan, Qi Cao, Keshan Wang and 13 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

50 citing papers in PubMed, 71 citations in OpenAlex.

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  12. No UCP1 in the kidney.Molecular metabolism · 2025
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  14. ATGL regulates renal fibrosis by reprogramming lipid metabolism during the transition from AKI to CKD.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors at 2 institutions in 1 country.

Zhiyong XiongDepartment of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Wen XiaoDepartment of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Lin BaoDepartment of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Wei XiongDepartment of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Haibing XiaoDepartment of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Yan QuDepartment of Pathogenic Biology School of Basic Medicine Huazhong University of Science and Technology Wuhan 430030 China.
Changfei YuanDepartment of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Hailong RuanDepartment of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Qi CaoDepartment of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Keshan WangDepartment of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Zhengshuai SongDepartment of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Cheng WangDepartment of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Wenjun HuDepartment of Pathogenic Biology School of Basic Medicine Huazhong University of Science and Technology Wuhan 430030 China.
Zeyuan RuDepartment of Pathogenic Biology School of Basic Medicine Huazhong University of Science and Technology Wuhan 430030 China.
Junwei TongDepartment of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Gong ChengDepartment of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Tianbo XuDepartment of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Xiangui MengDepartment of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Jian ShiDepartment of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Zhixian ChenDepartment of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Hongmei YangDepartment of Pathogenic Biology School of Basic Medicine Huazhong University of Science and Technology Wuhan 430030 China.
Ke ChenDepartment of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.ORCID https://orcid.org/0000-0002-2098-1921
Xiaoping ZhangDepartment of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Union Hospital · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging evidence has highlighted the important role of abnormal lipid accumulation in cancer development and progression, but the mechanism for this phenomenon remains unclear. Here, it is demonstrated that phospholipase C-like 1/uncoupling protein 1 (PLCL1)/(UCP1)-mediated lipid browning promotes tumor cell "slimming" and represses tumor progression. By screening three independent lipid metabolism-related gene sets in clear cell renal cell carcinoma (ccRCC) and analyzing the TCGA database, it is found that PLCL1 predicted a poor prognosis and was downregulated in ccRCC. Restoration of PLCL1 expression in ccRCC cells significantly represses tumor progression and reduces abnormal lipid accumulation. Additionally, a phenomenon called tumor cell "slimming," in which tumor cell volume is reduced and lipid droplets are transformed into tiny pieces, is observed. Further studies show that PLCL1 promotes tumor cell "slimming" and represses tumor progression through UCP1-mediated lipid browning, which consumes lipids without producing ATP energy. Mechanistic investigations demonstrate that PLCL1 improves the protein stability of UCP1 by influencing the level of protein ubiquitination. Collectively, the data indicate that lipid browning mediated by PLCL1/UCP1 promotes tumor cell "slimming" and consumes abnormal lipid accumulation, which represses the progression of ccRCC. Tumor cell "slimming" offers a promising new concept and treatment modality against tumor development and progression.

Indexed as

clear cell renal cell carcinomalipid browningPLCL1tumor cell “slimming”UCP1

Identifiers

PMID31131187
PMCPMC6523368
OpenAlexW2923568874

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.