Evidence map›Paper›PMID 33656238›Full record

ArticleJournal of cellular and molecular medicine2021

ERα down-regulates carbohydrate responsive element binding protein and decreases aerobic glycolysis in liver cancer cells.

Ying Lu, Na Tian, Lei Hu, Jian Meng, Ming Feng, Yemin Zhu, Ping Zhang, Minle Li, Qi Liu, Lingfeng Tong and 3 more

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

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 33% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.

  1. Pooled it
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  3. Article
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  5. Article
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

13 authors at 4 institutions in 1 country.

Ying LuDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Na TianDepartment of Neurology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Shandong, China.
Lei HuDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jian MengSchool of Clinical Medicine, Weifang Medical University, Weifang, China.
Ming FengSchool of Clinical Medicine, Weifang Medical University, Weifang, China.
Yemin ZhuDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ping ZhangDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Minle LiCancer Institute, Xuzhou Medical University, Xuzhou, China.
Qi LiuDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Lingfeng TongDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xuemei TongDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yakui LiDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Lifang WuDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0001-8730-9868
Shanghai Jiao Tong University · CNWeifang Medical University · CNShandong Provincial Hospital · CNXuzhou Medical College · CN

Funding

National Key Research and Development Program of China 2019YFA0906100National Natural Science Foundation of China 31601118National Natural Science Foundation of China 81302091National Natural Science Foundation of China 81472239National Natural Science Foundation of China 81672322National Natural Science Foundation of China 81972210National Natural Science Foundation of China 82003012National Natural Science Foundation of China 92057117Shanghai Municipal Science and Technology Major Project 19JC1410200The Program for Professor of Special Appointment (Eastern Scholar) at Shanghai Institutions of Higher Learning and Construction Plan of Laboratory Technical Team in Shanghai Universities SYjdyx18007
6 · The paper itself

Abstract

Deregulated metabolism is one of the characteristics of hepatocellular carcinoma. Sex hormone receptor signalling has been involved in the marked gender dimorphism of hepatocellular carcinoma pathogenesis. Oestrogen receptor (ER) has been reported to reduce the incidence of liver cancer. However, it remains unclear how oestrogen and ER regulate metabolic alterations in liver tumour cells. Our previous work revealed that ERα interacted with carbohydrate responsive element binding protein (ChREBP), which is a transcription factor promoting aerobic glycolysis and proliferation of hepatoma cells. Here, the data showed that ERα overexpression with E2 treatment reduced aerobic glycolysis and cell proliferation of hepatoma cells. In addition to modestly down-regulating ChREBP transcription, ERα promoted ChREBP degradation. ERα co-immunoprecipitated with both ChREBP-α and ChREBP-β, the two known subtypes of ChREBP. Although E2 promoted ERα to translocate to the nucleus, it did not change subcellular localization of ChREBP. In addition to interacting with ChREBP-β and promoting its degradation, ERα decreased ChREBP-α-induced ChREBP-β transcription. Taken together, we confirmed an original role of ERα in suppressing aerobic glycolysis in liver cancer cells and elucidated the mechanism by which ERα and ChREBP-α together regulated ChREBP-β expression.

Indexed as

Basic Helix-Loop-Helix Leucine Zipper Transcription FactorsCarcinoma, HepatocellularCell Line, TumorCell ProliferationDown-RegulationEstradiolEstrogen Receptor alphaGlycolysisHEK293 CellsHeLa CellsHep G2 CellsHumansLiver NeoplasmsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsEstradiolEstrogen Receptor alphaaerobic glycolysisChREBPERαliver cancerproliferation

Identifiers

PMID33656238
PMCPMC8034478
OpenAlexW3133662852

What OpenQuestion holds

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LicenceCC BY
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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.