Evidence map›Paper›PMID 38796854›Full record

ArticleCell reports2024

CRACD loss induces neuroendocrine cell plasticity of lung adenocarcinoma.

Bongjun Kim, Shengzhe Zhang, Yuanjian Huang, Kyung-Pil Ko, Youn-Sang Jung, Jinho Jang, Gengyi Zou, Jie Zhang, Sohee Jun, Kee-Beom Kim and 2 more

Abstract read
In one paragraph

Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Cell plasticity in cancer and therapy resistance.Experimental & molecular medicine · 2026
    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

12 authors.

Bongjun KimDepartment of Experimental Radiation Oncology, Division of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. Electronic address: bkim6@mdanderseon.org.
Shengzhe ZhangDepartment of Experimental Radiation Oncology, Division of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Yuanjian HuangDepartment of Experimental Radiation Oncology, Division of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Kyung-Pil KoDepartment of Experimental Radiation Oncology, Division of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Youn-Sang JungDepartment of Experimental Radiation Oncology, Division of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Jinho JangDepartment of Experimental Radiation Oncology, Division of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Gengyi ZouDepartment of Experimental Radiation Oncology, Division of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Jie ZhangDepartment of Experimental Radiation Oncology, Division of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Sohee JunDepartment of Experimental Radiation Oncology, Division of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Kee-Beom KimDepartment of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, VA 22908, USA; BK21 FOUR KNU Creative BioResearch Group, School of Life Sciences, Kyungpook National University, Daegu 41566, Republic of Korea.
Kwon-Sik ParkDepartment of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, VA 22908, USA.
Jae-Il ParkDepartment of Experimental Radiation Oncology, Division of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Graduate School of Biomedical Sciences, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Program in Genetics and Epigenetics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. Electronic address: jaeil@mdanderson.org.

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
PAF-Remodeled DREAM Complex in Cancer and RegenerationR01CA193297 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI PARK, JAE-IL · 2015 to 2024
$3.6M
CRACD-controlled cell plasticity and small cell lung cancerR01CA278967 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Jae-Il Park, Kwon-Sik Park · 2024 to 2026
$1.8M
Esophageal Squamous Cell Cancer Initiation and Immune Landscape RemodelingR01CA278971 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Jae-Il Park · 2024 to 2026
$1.7M
BD Biosciences Special Order LSRIIS10RR024574 · NCRR · BAYLOR COLLEGE OF MEDICINE · PI LUMPKIN, ELLEN A · 2009 to 2009
$430k
Modeling Esophageal Squamous Cell Cancer InitiationR03CA256207 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI PARK, JAE-IL · 2021 to 2022
$162k
Calcium metabolism and lung cancer preneoplasiaR03CA279867 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI PARK, JAE-IL · 2024 to 2025
$162k
NCI NIH HHS P30 CA016672NCI NIH HHS P30 CA125123NCI NIH HHS R01 CA193297NCI NIH HHS R01 CA278967NCI NIH HHS R01 CA278971NCI NIH HHS R03 CA256207NCI NIH HHS R03 CA279867NCRR NIH HHS S10 RR024574
6 · The paper itself

Abstract

Tumor cell plasticity contributes to intratumoral heterogeneity and therapy resistance. Through cell plasticity, some lung adenocarcinoma (LUAD) cells transform into neuroendocrine (NE) tumor cells. However, the mechanisms of NE cell plasticity remain unclear. CRACD (capping protein inhibiting regulator of actin dynamics), a capping protein inhibitor, is frequently inactivated in cancers. CRACD knockout (KO) is sufficient to de-repress NE-related gene expression in the pulmonary epithelium and LUAD cells. In LUAD mouse models, Cracd KO increases intratumoral heterogeneity with NE gene expression. Single-cell transcriptomic analysis showed that Cracd KO-induced NE cell plasticity is associated with cell de-differentiation and stemness-related pathway activation. The single-cell transcriptomic analysis of LUAD patient tumors recapitulates that the distinct LUAD NE cell cluster expressing NE genes is co-enriched with impaired actin remodeling. This study reveals the crucial role of CRACD in restricting NE cell plasticity that induces cell de-differentiation of LUAD.

Indexed as

Adenocarcinoma of LungCell PlasticityLung NeoplasmsNeuroendocrine CellsAnimalsCell Line, TumorGene Expression Regulation, NeoplasticHumansMiceMicrofilament ProteinsCracd protein, mouseMicrofilament ProteinsASCL1cell de-differentiationcell plasticityCP: CancerCRACDCRADKIAA1211lung adenocarcinomaneuroendocrine cell plasticitytherapy resistancetumor heterogeneity

Identifiers

PMID38796854
PMCPMC11216895

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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.