Evidence map›Paper›PMID 31218102›Full record

ArticleAmerican journal of cancer research2019

The miR-873/NDFIP1 axis promotes hepatocellular carcinoma growth and metastasis through the AKT/mTOR-mediated Warburg effect.

Yuyu Zhang, Chengbin Zhang, Qin Zhao, Wei Wei, Zhuo Dong, Lihong Shao, Jianbo Li, Wei Wu, Heng Zhang, He Huang and 2 more

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  5. PTEN: a new dawn in Parkinson's disease treatment.Frontiers in cellular neuroscience · 2025
    Review
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  11. Article
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  13. Article
  14. The Role of PI3K/AKT/mTOR Signaling in Hepatocellular Carcinoma Metabolism.International journal of molecular sciences · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

12 authors at 4 institutions in 1 country.

Yuyu ZhangNHC Key Laboratory of Radiobiology, Jilin University Changchun, China.
Chengbin ZhangDepartment of Pathology, The First Bethune Hospital of Jilin University Changchun, China.
Qin ZhaoDepartment of Radiation Oncology, The First Bethune Hospital of Jilin University Changchun, China.
Wei WeiNHC Key Laboratory of Radiobiology, Jilin University Changchun, China.
Zhuo DongNHC Key Laboratory of Radiobiology, Jilin University Changchun, China.
Lihong ShaoDepartment of Radiation Oncology, The First Bethune Hospital of Jilin University Changchun, China.
Jianbo LiDepartment of Histology and Embryology, Xiang Ya School of Medicine, Central South University Changsha, Hunan, China.
Wei WuDepartment of General Surgery, Xiangya Hospital, Central South University Changsha, Hunan, China.
Heng ZhangDepartment of Histology and Embryology, Xiang Ya School of Medicine, Central South University Changsha, Hunan, China.
He HuangDepartment of Histology and Embryology, Xiang Ya School of Medicine, Central South University Changsha, Hunan, China.
Feng LiuDepartment of Nephrology, China-Japan Union Hospital of Jilin University Changchun, China.
Shunzi JinNHC Key Laboratory of Radiobiology, Jilin University Changchun, China.
Central South University · CNJilin University · CNFirst Bethune Hospital of Jilin University · CNUnion Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) progression depends on cellular metabolic reprogramming as both direct and indirect consequence of oncogenic lesions. However, the underlying mechanisms are still understood poorly. Here, we report that miR-873 promotes Warburg effect in HCC cells by increasing glucose uptake, extracellular acidification rate (ECAR), lactate production, and ATP generation, and decreasing oxygen consumption rate (OCR) in HCC cells. Mechanistically, we show that miR-873 activates the key glycolytic proteins AKT/mTOR via targeting NDFIP1 which triggers metabolic shift. We further demonstrate that enhanced glycolysis is essential for the role of miR-873 to drive HCC progression. By using immunohistochemistry analysis, we show a link between the aberrant expression of miR-873, NDFIP1, and phospho-AKT in clinical HCC samples. We also found that miR-873 was up-regulated by HIF1α, a critical glycolysis-related transcription factor. However, BAY 87-2243, a HIF1α specific inhibitor, blocks miR-873 mediated tumor growth and metastasis in nude mice. Collectively, our data uncover a previously unappreciated function of miR-873 in HCC cell metabolism and tumorigenesis, suggesting that targeting miR-873/NDFIP1 axis could be a potential therapeutic strategy for the treatment of HCC patients.

Indexed as

HCCmiR-873NDFIP1Warburg effect

Identifiers

PMID31218102
PMCPMC6556606
OpenAlexW3006227236

What OpenQuestion holds

Textmetadata
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.