Evidence map›Paper›PMID 31315616›Full record

ArticleCell communication and signaling : CCS2019

NR6A1 regulates lipid metabolism through mammalian target of rapamycin complex 1 in HepG2 cells.

Yinfang Wang, Xiaohong Wan, Yilong Hao, Yuanyuan Zhao, Lanlan Du, Yitong Huang, Zongjun Liu, Ying Wang, Nanping Wang, Peng Zhang

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

22 citing papers in PubMed, 31 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

10 authors at 3 institutions in 2 countries.

Yinfang WangShanghai Putuo Central School of Clinical Medicine, Anhui Medical University, Hefei, 230001, China. wngynfng@163.com.
Xiaohong WanShanghai Putuo Central School of Clinical Medicine, Anhui Medical University, Hefei, 230001, China.
Yilong HaoCentral Laboratory, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200062, China.
Yuanyuan ZhaoCentral Laboratory, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200062, China.
Lanlan DuDepartment of Cardiovascular Medicine, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200062, China.
Yitong HuangCentral Laboratory, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200062, China.
Zongjun LiuDepartment of Cardiovascular Medicine, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200062, China.
Ying WangDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Florida, 32224, USA.
Nanping WangThe Advanced Institute for Medical Sciences, Dalian Medical University, Dalian, 116044, China.
Peng ZhangShanghai Putuo Central School of Clinical Medicine, Anhui Medical University, Hefei, 230001, China. zhangnep@hotmail.com.
Shanghai University of Traditional Chinese Medicine · CNAnhui Medical University · CNDalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLipogenesis is required for the optimal growth of many types of cancer cells, it is shown to control the biosynthesis of the lipid bilayer membrane during rapid proliferation and metastasis, provides cancer cells with signaling lipid molecules to support cancer development and make cancer cells more resistant to oxidative stress-induced cell death. Though multiple lipogenic enzymes have been identified to mediate this metabolic change, how the expression of these lipogenic enzymes are transcriptionally regulated remains unclear.

methodsGain- and loss-of-function experiments were conducted to assess the role of transcriptional repressor, nuclear receptor sub-family 6, group A, member 1 (NR6A1) in HepG2 cells. RT-qPCR method was performed to investigate target gene of NR6A1. Western blot was employed to determine the mechanisms by which NR6A1 regulates lipid accumulation in HepG2 cells.

resultsWe provide evidence that NR6A1 is a novel regulator of lipid metabolism in HepG2 cells. NR6A1 knockdown can increase lipid accumulation as well as insulin-induced proliferation and migration of HepG2 cells. The lipogenic effect correlated well with the expression of lipogenic genes, including fatty acid synthase (FAS), diglyceride acyltransferase-2 (DGAT2), malic enzyme 1 (ME1), microsomal triglyceride transfer protein (MTTP) and phosphoenolpyruvate carboxykinase (PEPCK). NR6A1 knockdown also increased the expression of carnitine palmitoyltransferase 1A (CPT1a), the rate-limiting enzyme in fatty acid oxidation. Furthermore, NR6A1 knockdown induced lipid accumulation through mammalian target of rapamycin complex 1 (mTORC1), but not mTORC2. Moreover, siRNA-mediated knockdown of NR6A1 increased expression of insulin receptor (INSR) and potentitated insulin-induced phosphorylation of mTOR and AKT partly via miR-205-5p in HepG2 cells.

conclusionsThese findings provide important new insights into the role of NR6A1 in the lipogenesis in HepG2 cells. .

Indexed as

Lipid MetabolismAnimalsCell MovementCell ProliferationGene Expression RegulationGene SilencingHEK293 CellsHep G2 CellsHumansInsulinLipogenesisMechanistic Target of Rapamycin Complex 1MicroRNAsNuclear Receptor Subfamily 6, Group A, Member 1Receptor, InsulinSignal TransductionInsulinMechanistic Target of Rapamycin Complex 1MicroRNAsMIR205, humanNR6A1 protein, humanNuclear Receptor Subfamily 6, Group A, Member 1Receptor, InsulinHepG2 cellsInsulin receptorLipogenesismiR-205-5pNR6A1

Identifiers

PMID31315616
PMCPMC6637573
OpenAlexW2960078707

What OpenQuestion holds

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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.