Evidence map›Paper›PMID 35436988›Full record

ArticleCell discovery2022

Cell-in-cell structure mediates in-cell killing suppressed by CD44.

Yan Su, Hongyan Huang, Tianzhi Luo, You Zheng, Jie Fan, He Ren, Meng Tang, Zubiao Niu, Chenxi Wang, Yuqi Wang and 8 more

Open access · goldAbstract read
In one paragraph

Article in Cell discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  6. The battle within: cell death by phagocytosis in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
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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

18 authors at 5 institutions in 3 countries.

Yan Su *Beijing Institute of Biotechnology, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, 20 Dongda Street, Beijing, China.
Hongyan Huang *Department of Oncology, Beijing Shijitan Hospital of Capital Medical University, Beijing, China.ORCID http://orcid.org/0000-0001-8340-6660
Tianzhi Luo *CAS Key Laboratory of Mechanical Behavior and Design of Materials, Department of Modern Mechanics, University of Science and Technology of China, Hefei, China.
You ZhengBeijing Institute of Biotechnology, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, 20 Dongda Street, Beijing, China.
Jie FanBeijing Institute of Biotechnology, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, 20 Dongda Street, Beijing, China.
He RenBeijing Institute of Biotechnology, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, 20 Dongda Street, Beijing, China.
Meng TangBeijing Institute of Biotechnology, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, 20 Dongda Street, Beijing, China.
Zubiao NiuBeijing Institute of Biotechnology, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, 20 Dongda Street, Beijing, China.
Chenxi WangBeijing Institute of Biotechnology, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, 20 Dongda Street, Beijing, China.
Yuqi WangBeijing Institute of Biotechnology, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, 20 Dongda Street, Beijing, China.
Zhengrong ZhangBeijing Institute of Biotechnology, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, 20 Dongda Street, Beijing, China.
Jianqing LiangBeijing Institute of Biotechnology, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, 20 Dongda Street, Beijing, China.
Banzhan RuanBeijing Institute of Biotechnology, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, 20 Dongda Street, Beijing, China.
Lihua GaoBeijing Institute of Biotechnology, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, 20 Dongda Street, Beijing, China.
Zhaolie ChenBeijing Institute of Biotechnology, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, 20 Dongda Street, Beijing, China.
Gerry MelinoDepartments of Experimental Medicine, University of Rome Tor Vergata, Rome, Italy.ORCID http://orcid.org/0000-0001-9428-5972
Xiaoning WangNational Research Center of Geriatrics Diseases, Chinese PLA General Hospital, Beijing, China.
Qiang SunBeijing Institute of Biotechnology, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, 20 Dongda Street, Beijing, China. sunq@bmi.ac.cn.ORCID http://orcid.org/0000-0002-5342-0637
Chinese Academy of Medical Sciences & Peking Union Medical College · CNCapital Medical University · CNUniversity of Science and Technology of China · CNChinese PLA General Hospital · CNUniversity of Rome Tor Vergata · IT

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31970685National Natural Science Foundation of China (National Science Foundation of China) 81872314
6 · The paper itself

Abstract

Penetration of immune cells into tumor cells was believed to be immune-suppressive via cell-in-cell (CIC) mediated death of the internalized immune cells. We unexpectedly found that CIC formation largely led to the death of the host tumor cells, but not the internalized immune cells, manifesting typical features of death executed by NK cells; we named this "in-cell killing" which displays the efficacy superior to the canonical way of "kiss-killing" from outside. By profiling isogenic cells, CD44 on tumor cells was identified as a negative regulator of "in-cell killing" via inhibiting CIC formation. CD44 functions to antagonize NK cell internalization by reducing N-cadherin-mediated intercellular adhesion and by enhancing Rho GTPase-regulated cellular stiffness as well. Remarkably, antibody-mediated blockade of CD44 signaling potentiated the suppressive effects of NK cells on tumor growth associated with increased heterotypic CIC formation. Together, we identified CIC-mediated "in-cell killing" as a promising strategy for cancer immunotherapy.

Identifiers

PMID35436988
PMCPMC9016064
OpenAlexW4224241797

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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.