Evidence map›Paper›PMID 41438579›Full record

ArticleJournal of Cancer2026

CES3 promotes NSCLC progression via lipid metabolic reprogramming regulated by TFAP2A.

Pengfei Luo, Zirui Huang, Sijuan Ding, Zhangwen Tang, Yanhong Wei, Shaohui Jiang, Ruoting Tang, Fang Li, Han Yang, Lujun Zhao

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of Cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Pengfei LuoDepartment of Radiation Oncology, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin 300060, China.
Zirui HuangState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Sijuan DingDepartment of Oncology, The Central Hospital of Yongzhou, No. 396 Yiyun Road, Yongzhou City, 425000 Hunan Province, China. Hunan Provincial Demonstration Base for Medical Technology in Tumor Radiotherapy.
Zhangwen TangDepartment of Oncology, The Central Hospital of Yongzhou, No. 396 Yiyun Road, Yongzhou City, 425000 Hunan Province, China. Hunan Provincial Demonstration Base for Medical Technology in Tumor Radiotherapy.
Yanhong WeiDepartment of Oncology, The Central Hospital of Yongzhou, No. 396 Yiyun Road, Yongzhou City, 425000 Hunan Province, China. Hunan Provincial Demonstration Base for Medical Technology in Tumor Radiotherapy.
Shaohui JiangDepartment of Oncology, The Central Hospital of Yongzhou, No. 396 Yiyun Road, Yongzhou City, 425000 Hunan Province, China. Hunan Provincial Demonstration Base for Medical Technology in Tumor Radiotherapy.
Ruoting TangDepartment of Oncology, The Central Hospital of Yongzhou, No. 396 Yiyun Road, Yongzhou City, 425000 Hunan Province, China. Hunan Provincial Demonstration Base for Medical Technology in Tumor Radiotherapy.
Fang LiDepartment of Oncology, The Central Hospital of Yongzhou, No. 396 Yiyun Road, Yongzhou City, 425000 Hunan Province, China. Hunan Provincial Demonstration Base for Medical Technology in Tumor Radiotherapy.
Han YangState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Lujun ZhaoDepartment of Radiation Oncology, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin 300060, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic reprogramming is an important feature in non-small cell lung cancer (NSCLC) that can result in therapeutic resistance. Exploring dysregulated lipid metabolism in NSCLC will accelerate the development of potential lipid biomarkers to target and control the malignant progression of NSCLC. In this study, RNA next-generation sequencing of 25 paired NSCLC specimens and adjacent normal tissues was used to find that carboxylesterase 3 (CES3) was upregulated in NSCLC. Knockdown of CES3 significantly inhibited NSCLC cell proliferation and invasion. Additionally, CES3 inhibition promoted lipid accumulation in NSCLC cells. Furthermore, we found transcription factor AP-2α (TFAP2A) could regulate CES3 levels in NSCLC. TFAP2A was found upregulated in NSCLC and correlated with poorer outcome. Inhibiting TFAP2A resulted in suppressed cell proliferation as well as invasion while increasing the lipid accumulation in NSCLC. CES3 overexpression could reverse the impact of TFAP2A inhibition on NSCLC progression. In summary, TFAP2A dysregulation resulted in CES3 overexpression and the following NSCLC tumorigenesis. Targeting the TFAP2A/CES3 axis may represent a promising therapeutic strategy for NSCLC in the future.

Indexed as

carboxylesterase 3lipid metabolismnon-small cell lung cancerproliferationtranscription factor AP-2α

Identifiers

PMID41438579
PMCPMC12719574

What Socratic holds

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LicenceCC BY
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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 Socratic graph.