Evidence map›Paper›PMID 35428350›Full record

ArticleCell death & disease2022

EGFR/MET promotes hepatocellular carcinoma metastasis by stabilizing tumor cells and resisting to RTKs inhibitors in circulating tumor microemboli.

Shouyang Song, Zhen Yu, Yajing You, Chenxi Liu, Xiaoyu Xie, Huanran Lv, Feng Xiao, Qiang Zhu, Chengyong Qin

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Single-Molecule FRET-Tracking of InlB-Activated MET Receptors in Living Cells.Small (Weinheim an der Bergstrasse, Germany) · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Hepatocellular carcinoma: signaling pathways and therapeutic advances.Signal transduction and targeted therapy · 2025
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. 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

9 authors at 3 institutions in 1 country.

Shouyang SongShandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, P.R. China.
Zhen YuShandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, P.R. China.
Yajing YouShandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, P.R. China.
Chenxi LiuShandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, P.R. China.
Xiaoyu XieShandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, P.R. China.
Huanran LvShandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, P.R. China.
Feng XiaoShandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, P.R. China.
Qiang ZhuShandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, P.R. China. zhuqiang@sdu.edu.cn.ORCID 0000-0002-5843-9724
Chengyong QinShandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, P.R. China. chengyong_qin@126.com.ORCID 0000-0002-0930-943X
Shandong University · CNShandong Provincial Hospital · CNXinjiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The receptor tyrosine kinases (RTKs) family is well-recognized as vital targets for the treatment of hepatocarcinoma cancer (HCC) clinically, whereas the survival benefit of target therapy sorafenib is not satisfactory for liver cancer patients due to metastasis. EGFR and MET are two molecules of the RTK family that were related to the survival time of liver cancer patients and resistance to targeted therapy in clinical reports. However, the mechanism and clinical therapeutic value of EGFR/MET in HCC metastasis are still not completely clarified. The study confirmed that EGFR/MET was highly expressed in HCC cells and tissues and the phosphorylation was stable after metastasis. The expression of EGFR/MET was up-regulated in circulating tumor microemboli (CTM) to accelerate IL-8 production and resistance to the lethal effect of leukocytes. Meanwhile, highly expressed EGFR/MET effectively regulated the Ras/MAPK pathway and stabilized suspended HCC cells by facilitating proliferation and inhibiting apoptosis. Moreover, EGFR/MET promoted phosphorylation of hetero-RTKs, which was dependent on high-energy phosphoric acid compounds rather than their direct interactions. In conclusion, highly expressed EGFR/MET could be used in CTM identification and suitable for preventing metastasis of HCC in clinical practice.

Indexed as

Carcinoma, HepatocellularErbB ReceptorsLiver NeoplasmsProto-Oncogene Proteins c-metCell Line, TumorDrug Resistance, NeoplasmHumansNeoplasm MetastasisProtein Kinase InhibitorsReceptor Protein-Tyrosine KinasesSorafenibEGFR protein, humanErbB ReceptorsMET protein, humanProtein Kinase InhibitorsProto-Oncogene Proteins c-metReceptor Protein-Tyrosine KinasesSorafenib

Identifiers

PMID35428350
PMCPMC9012802
OpenAlexW4224084840

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.