Evidence map›Paper›PMID 32019286›Full record

ArticleCancer research and treatment2020

Activation of Tyrosine Metabolism in CD13+ Cancer Stem Cells Drives Relapse in Hepatocellular Carcinoma.

Li Sun, Lin Zhang, Jun Chen, Chaoqun Li, Hongqin Sun, Jiangrong Wang, Hong Xiao

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

Article in Cancer research and treatment, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 49 citations in OpenAlex.

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  14. Application of Metabolic Reprogramming to Cancer Imaging and Diagnosis.International journal of molecular sciences · 2022
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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

7 authors at 2 institutions in 1 country.

Li SunDepartment of Oncology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Lin ZhangThe Nursing Department, Shanghai Public Health Clinical Center, Shanghai, China.
Jun ChenThe First Department of Infectious Diseases, Shanghai Public Health Clinical Center, Shanghai, China.
Chaoqun LiThe Third Department of Infectious Diseases, Shanghai Public Health Clinical Center, Shanghai, China.
Hongqin SunThe Third Department of Infectious Diseases, Shanghai Public Health Clinical Center, Shanghai, China.
Jiangrong WangThe First Department of Infectious Diseases, Shanghai Public Health Clinical Center, Shanghai, China.
Hong XiaoThe Third Department of Infectious Diseases, Shanghai Public Health Clinical Center, Shanghai, China.
Shanghai Public Health Clinical Center · CNRenji Hospital · CN

Funding

Funds of the Shanghai Board of Health 184080
6 · The paper itself

Abstract

purposeCancer stem cells (CSCs) are naturally resistant to chemotherapy, explaining why tumor relapse frequently occurs after initial regression upon administration of chemotherapeutic agents in most cases. A CSC population characterized by CD13 expression has been identified in hepatocellular carcinoma (HCC). In the current study, we aimed to clarify the molecular mechanism by which it escapes conventional therapies. MATERIALS AND

methodsHere, we used flow cytometry to examine the percentage of CD13+ CSCs in HepG2 and HuH7 cells after chemotherapy. Using in vitro isotope labeling technique, we compared metabolic pathways between CD13+ and CD13- subpopulations. Using co-immunoprecipitation and western blotting, we determined the target expressions in protein levels under different conditions. We also performed immunohistochemistry to detect the target proteins under different conditions. Animal models were constructed to verify the potential role of tyrosine metabolism in post-chemotherapeutic relapse in vivo.

resultsWe observed that quiescent CD13+ CSCs are enriched after chemotherapy in HCCs, and serve as a reservoir for recurrence. Mechanistically, CD13+ CSCs were dependent on aerobic metabolism of tyrosine rather than glucose as energy source. Tyrosine metabolism also generated nuclear acetyl-CoA to acetylate and stabilize Foxd3, thereby allowing CD13+ CSCs cells to sustain quiescence and resistance to chemotherapeutic agents.

conclusionThese findings encourage further exploration of eliminating CD13+ cells by targeting specific metabolic pathways to prevent recurrence in HCCs.

Indexed as

AnimalsCarcinoma, HepatocellularCD13 AntigensHumansLiver NeoplasmsMiceMice, NudeNeoplastic Stem CellsRecurrenceTyrosineCD13 AntigensTyrosineCD13+ CSCsFoxd3Hepatocellular carcinomaQuiescenceTyrosine metabolism

Identifiers

PMID32019286
PMCPMC7176959
OpenAlexW2997755446

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.