Evidence map›Paper›PMID 38560575›Full record

ArticleOncology research2024

Degradation of FAK-targeting by proteolytic targeting chimera technology to inhibit the metastasis of hepatocellular carcinoma.

Xinfeng Zhang, Shuang Li, Meiru Song, Yue Chen, Liangzheng Chang, Zherui Liu, Hongyuan Dai, Yutao Wang, Gangqi Yang, Yun Jiang and 1 more

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

Article in Oncology research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. 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

11 authors at 1 institution in 1 country.

Xinfeng ZhangThe PLA 307 Clinical College of Anhui Medical University, The Fifth Clinical Medical College of Anhui Medical University, Hefei, 230032, China.
Shuang LiLiver Tumor Diagnosis and Research Center, 5th Medical Center of the PLA General Hospital, Beijing, 100039, China.
Meiru SongThe PLA 307 Clinical College of Anhui Medical University, The Fifth Clinical Medical College of Anhui Medical University, Hefei, 230032, China.
Yue ChenDepartment of Infection Diseases, Guizhou Medical University, Guiyang, 550025, China.
Liangzheng ChangDepartment of Infection Diseases, Guizhou Medical University, Guiyang, 550025, China.
Zherui Liu302 Clinical Medical School, Peking University, Beijing, China.
Hongyuan DaiDepartment of Infection Diseases, Guizhou Medical University, Guiyang, 550025, China.
Yutao Wang302 Clinical Medical School, Peking University, Beijing, China.
Gangqi YangDepartment of Infection Diseases, Guizhou Medical University, Guiyang, 550025, China.
Yun JiangCell and Gene Therapy Innovation Center, Beijing Lotuslake Biomedical, Science and Technology Park, Beijing, 102206, China.
Yinying LuThe PLA 307 Clinical College of Anhui Medical University, The Fifth Clinical Medical College of Anhui Medical University, Hefei, 230032, China.
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver cancer is a prevalent malignant cancer, ranking third in terms of mortality rate. Metastasis and recurrence primarily contribute to the high mortality rate of liver cancer. Hepatocellular carcinoma (HCC) has low expression of focal adhesion kinase (FAK), which increases the risk of metastasis and recurrence. Nevertheless, the efficacy of FAK phosphorylation inhibitors is currently limited. Thus, investigating the mechanisms by which FAK affects HCC metastasis to develop targeted therapies for FAK may present a novel strategy to inhibit HCC metastasis. This study examined the correlation between FAK expression and the prognosis of HCC. Additionally, we explored the impact of FAK degradation on HCC metastasis through wound healing experiments, transwell invasion experiments, and a xenograft tumor model. The expression of proteins related to epithelial-mesenchymal transition (EMT) was measured to elucidate the underlying mechanisms. The results showed that FAK PROTAC can degrade FAK, inhibit the migration and invasion of HCC cells

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionFocal Adhesion Protein-Tyrosine KinasesGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessNeoplasm MetastasisPrognosisFocal Adhesion Protein-Tyrosine KinasesEpithelial-mesenchymal transformation (EMT)Focal adhesion kinase (FAK)Hepatocellular carcinoma (HCC)MetastasisProteolytic targeting chimera technology (PROTAC)

Identifiers

PMID38560575
PMCPMC10972732
OpenAlexW4391758756

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.