Evidence map›Paper›PMID 31358770›Full record

ArticleNature communications2019

ER-residential Nogo-B accelerates NAFLD-associated HCC mediated by metabolic reprogramming of oxLDL lipophagy.

Yuan Tian, Bin Yang, Weinan Qiu, Yajing Hao, Zhenxing Zhang, Bo Yang, Nan Li, Shuqun Cheng, Zhangjun Lin, Yao-Cheng Rui and 11 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

71 citing papers in PubMed, 107 citations in OpenAlex.

  1. Advances in Lipid Metabolism Reprogramming in Hepatocellular Carcinoma.Journal of clinical and translational hepatology · 2026
    Review
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  10. Molecular mechanisms in MASLD/MASH-related HCC.Hepatology (Baltimore, Md.) · 2025
    Review
  11. Lipids: Driving Forces in the Underlying Biology of Carcinogenesis.ACS pharmacology & translational science · 2025
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Unveiling the cancer risk nexus of the steatotic liver.Trends in endocrinology and metabolism: TEM · 2024
    Review

11 more citing papers are in PubMed but not listed here.

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

21 authors at 5 institutions in 1 country.

Yuan TianKey Laboratory of Infection and Immunity of CAS, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Bin YangKey Laboratory of Infection and Immunity of CAS, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Weinan QiuKey Laboratory of Infection and Immunity of CAS, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Yajing HaoUniversity of Chinese Academy of Sciences, 100049, Beijing, China.
Zhenxing ZhangKey Laboratory of Infection and Immunity of CAS, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Bo YangKey Laboratory of Infection and Immunity of CAS, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Nan LiEastern Hepatobiliary Surgery Hospital, Second Military Medical University, 200433, Shanghai, China.
Shuqun ChengEastern Hepatobiliary Surgery Hospital, Second Military Medical University, 200433, Shanghai, China.
Zhangjun LinKey Laboratory of Infection and Immunity of CAS, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Yao-Cheng RuiDepartment of Pharmacology and School of Pharmacy, Second Military Medical University, 200433, Shanghai, China.
Otto K W CheungSchool of Biomedical Sciences, The Chinese University of Hong Kong, 999077, Hong Kong, China.
Weiqin YangSchool of Biomedical Sciences, The Chinese University of Hong Kong, 999077, Hong Kong, China.
William K K WuState Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, 999077, Hong Kong, China.
Yue-Sun CheungDepartment of Surgery, The Chinese University of Hong Kong, 999077, Hong Kong, China.
Paul B S LaiDepartment of Surgery, The Chinese University of Hong Kong, 999077, Hong Kong, China.
Jianjun LuoKey Laboratory of RNA Biology of CAS, Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Joseph J Y SungState Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, 999077, Hong Kong, China.
Runsheng ChenKey Laboratory of RNA Biology of CAS, Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Hong-Yang WangEastern Hepatobiliary Surgery Hospital, Second Military Medical University, 200433, Shanghai, China.
Alfred S L ChengSchool of Biomedical Sciences, The Chinese University of Hong Kong, 999077, Hong Kong, China. alfredcheng@cuhk.edu.hk.
Pengyuan YangKey Laboratory of Infection and Immunity of CAS, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China. pyyang@ibp.ac.cn.
Chinese University of Hong Kong · CNInstitute of Biophysics · CNSecond Military Medical University · CNChinese Academy of Sciences · CNUniversity of Chinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome that elevates the risk of hepatocellular carcinoma (HCC). Although alteration of lipid metabolism has been increasingly recognized as a hallmark of cancer cells, the deregulated metabolic modulation of HCC cells in the NAFLD progression remains obscure. Here, we discovers an endoplasmic reticulum-residential protein, Nogo-B, as a highly expressed metabolic modulator in both murine and human NAFLD-associated HCCs, which accelerates high-fat, high-carbohydrate diet-induced metabolic dysfunction and tumorigenicity. Mechanistically, CD36-mediated oxLDL uptake triggers CEBPβ expression to directly upregulate Nogo-B, which interacts with ATG5 to promote lipophagy leading to lysophosphatidic acid-enhanced YAP oncogenic activity. This CD36-Nogo-B-YAP pathway consequently reprograms oxLDL metabolism and induces carcinogenetic signaling for NAFLD-associated HCCs. Targeting the Nogo-B pathway may represent a therapeutic strategy for HCC arising from the metabolic syndrome.

Indexed as

AutophagyAnimalsCarcinoma, HepatocellularCell Line, TumorDiet, High-FatEndoplasmic ReticulumFemaleGene Expression ProfilingHep G2 CellsHumansKaplan-Meier EstimateLipoproteins, LDLLiver NeoplasmsMetabolic SyndromeMice, Inbred C57BLMice, NudeLipoproteins, LDLNogo Proteinsoxidized low density lipoprotein

Identifiers

PMID31358770
PMCPMC6662851
OpenAlexW2964829737

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.