Evidence map›Paper›PMID 38744820›Full record

ArticleNature communications2024

Dysfunctional adipocytes promote tumor progression through YAP/TAZ-dependent cancer-associated adipocyte transformation.

Yaechan Song, Heeju Na, Seung Eon Lee, You Min Kim, Jihyun Moon, Tae Wook Nam, Yul Ji, Young Jin, Jae Hyung Park, Seok Chan Cho and 6 more

Erratum issuedAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 2 pooled it
–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

29 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. [Recent Advances in the Interorgan Regulatory Roles of Adipose Tissue].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026
    Pooled it
  2. Pooled it
  3. Energy Balance-Related Factors and Direct Tumor-Adipocyte Contact in Colorectal Cancer: Etiologic Insights from the Population-Based Netherlands Cohort Study.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors.

Yaechan Song *Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea.ORCID http://orcid.org/0000-0001-5172-5659
Heeju Na *Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea.
Seung Eon LeeDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea.
You Min KimDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea.
Jihyun MoonDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea.
Tae Wook NamDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea.
Yul JiDepartment of Biological Sciences, Seoul National University, Seoul, 08826, Republic of Korea.
Young JinDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea.
Jae Hyung ParkDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea.
Seok Chan ChoDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea.
Jaehoon LeeDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea.ORCID http://orcid.org/0000-0001-9777-5918
Daehee HwangDepartment of Biological Sciences, Seoul National University, Seoul, 08826, Republic of Korea.
Sang-Jun HaDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea.ORCID http://orcid.org/0000-0002-1192-6031
Hyun Woo ParkDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea.ORCID http://orcid.org/0000-0001-7736-2286
Jae Bum KimDepartment of Biological Sciences, Seoul National University, Seoul, 08826, Republic of Korea.ORCID http://orcid.org/0000-0003-2337-6935
Han-Woong LeeDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea. hwl@yonsei.ac.kr.ORCID http://orcid.org/0000-0001-9515-3605

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity has emerged as a prominent risk factor for the development of malignant tumors. However, the existing literature on the role of adipocytes in the tumor microenvironment (TME) to elucidate the correlation between obesity and cancer remains insufficient. Here, we aim to investigate the formation of cancer-associated adipocytes (CAAs) and their contribution to tumor growth using mouse models harboring dysfunctional adipocytes. Specifically, we employ adipocyte-specific BECN1 KO (BaKO) mice, which exhibit lipodystrophy due to dysfunctional adipocytes. Our results reveal the activation of YAP/TAZ signaling in both CAAs and BECN1-deficient adipocytes, inducing adipocyte dedifferentiation and formation of a malignant TME. The additional deletion of YAP/TAZ from BaKO mice significantly restores the lipodystrophy and inflammatory phenotypes, leading to tumor regression. Furthermore, mice fed a high-fat diet (HFD) exhibit decreased BECN1 and increased YAP/TAZ expression in their adipose tissues. Treatment with the YAP/TAZ inhibitor, verteporfin, suppresses tumor progression in BaKO and HFD-fed mice, highlighting its efficacy against mice with metabolic dysregulation. Overall, our findings provide insights into the key mediators of CAA and their significance in developing a TME, thereby suggesting a viable approach targeting adipocyte homeostasis to suppress cancer growth.

Indexed as

Adaptor Proteins, Signal TransducingAdipocytesDiet, High-FatMice, KnockoutTranscriptional Coactivator with PDZ-Binding Motif ProteinsTumor MicroenvironmentYAP-Signaling ProteinsAnimalsCell Cycle ProteinsCell Transformation, NeoplasticDisease ProgressionLipodystrophyMiceMice, Inbred C57BLNeoplasmsObesityAdaptor Proteins, Signal TransducingCell Cycle ProteinsTrans-ActivatorsTranscriptional Coactivator with PDZ-Binding Motif ProteinsTranscription FactorsVerteporfinYAP-Signaling Proteins

Identifiers

PMID38744820
PMCPMC11094189

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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.