Evidence map›Paper›PMID 39415235›Full record

ArticleJournal of translational medicine2024

STYK1 mediates NK cell anti-tumor response through regulating CCR2 and trafficking.

Junming He, Yuexi He, Ruojia Biao, Yuqing Wei, Zhongjun Dong, Juan Du

Abstract read
In one paragraph

Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Cellular crosstalk in the bone marrow niche.Journal of translational medicine · 2024
    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

6 authors.

Junming HeBeijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University, Beijing, 102218, China.
Yuexi HeState Key Laboratory of Membrane Biology, School of Medicine and Institute for Immunology, Tsinghua University, Beijing, 100084, China.
Ruojia BiaoNational Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing, 100015, China.
Yuqing WeiNational Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing, 100015, China.
Zhongjun DongDepartment of Allergy, The First Affiliated Hospital of Anhui Medical University and Institute of Clinical Immunology, Anhui Medical University, Hefei, 230032, China. dongzj@mail.tsinghua.edu.cn.
Juan DuNational Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing, 100015, China. duj656@ccmu.edu.cn.

Funding

Beijing Natural Science Foundation M21007China Postdoctoral Science Foundation 2020M670296China Postdoctoral Science Foundation 2021T140372National Natural Science Foundation of China 81902895National Natural Science Foundation of China 82371565
6 · The paper itself

Abstract

The serine/threonine/tyrosine kinase 1 (STYK1) is a receptor protein-tyrosine kinase (RPTK)-like molecule that is detected in several human organs. STYK1 plays an important role in promoting tumorigenesis and metastasis in various cancers. By analyzing the expression of RTKs in immune cells in the database of 2013 Immunological Genome Project, we found that STYK1 was principally expressed in NK cells. In order to investigate the function of STYK1, we used CRISPR/Cas9 technology to generate STYK1-deleted mice, we found STYK1 deletion mice have normal number, development, and function of NK cells in spleen and bone marrow in tumor-free resting state. To examine the tumor surveillance of STYK1 in vivo, we utilized a variety of tumor models, including NK cell-specific target cell (ß2M and RMA-S) clearance experiments in vivo, subcutaneous and intravenous injection of B16F10 melanoma model, and the spontaneous breast cancer model MMTV-PyMT. Surprisingly, we discovered that deletion of the oncogenic STYK1 promoted the four-model tumor progression, and we observed a reduction of NK cell accumulation in the tumor tissues of STYK1 deletion mice compared to WT mice. In order to study the mechanism of STYK1 in NK, RNA sequence of STYK1

Indexed as

Cell MovementKiller Cells, NaturalReceptor Protein-Tyrosine KinasesReceptors, CCR2AnimalsCell Line, TumorFemaleGene DeletionHumansMelanoma, ExperimentalMiceMice, Inbred C57BLMice, KnockoutNeoplasmsReceptor Protein-Tyrosine KinasesReceptors, CCR2Styk1 protein, mouseCCR2Natural killer (NK) cellsProgressionSerine/threonine/tyrosine kinase 1 (STYK1)Tumor infiltrating

Identifiers

PMID39415235
PMCPMC11481722

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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.