Evidence map›Paper›PMID 41319185›Full record

ArticleCancer biology & therapy2025

NCAPD2 promotes the progression of lung adenocarcinoma through an AKT/MDM2/E2F1 positive feedback loop.

Yun Wu, Xiaoqin Li, Yuchen Lin, Yan Chen, Ning Xin, Da Hong, Junmin Wei, Hongru Li, Tailin Guo, Fan Lin and 2 more

Abstract read
In one paragraph

Article in Cancer biology & therapy, 2025. 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

12 authors.

Yun WuFujian Provincial Center for Geriatrics, Fuzhou University Affiliated Provincial Hospital, Fuzhou, China.ORCID 0009-0000-9590-021X
Xiaoqin LiShengli Clinical Medical College of Fujian Medical University, Fuzhou, China.
Yuchen LinThe School of Nursing, Fujian Medical University, Fuzhou, China.
Yan ChenFujian Provincial Center for Geriatrics, Fuzhou University Affiliated Provincial Hospital, Fuzhou, China.
Ning XinFujian Provincial Center for Geriatrics, Fuzhou University Affiliated Provincial Hospital, Fuzhou, China.
Da HongFujian Provincial Center for Geriatrics, Fuzhou University Affiliated Provincial Hospital, Fuzhou, China.
Junmin WeiFujian Provincial Center for Geriatrics, Fuzhou University Affiliated Provincial Hospital, Fuzhou, China.
Hongru LiShengli Clinical Medical College of Fujian Medical University, Fuzhou, China.
Tailin GuoFujian Provincial Center for Geriatrics, Fuzhou University Affiliated Provincial Hospital, Fuzhou, China.
Fan LinFujian Provincial Center for Geriatrics, Fuzhou University Affiliated Provincial Hospital, Fuzhou, China.
Yusheng ChenShengli Clinical Medical College of Fujian Medical University, Fuzhou, China.
Ying LinShengli Clinical Medical College of Fujian Medical University, Fuzhou, China.ORCID 0000-0002-1280-2102

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionLung adenocarcinoma (LUAD) is one of the leading causes of cancer-related deaths worldwide. While NCAPD2 has been implicated in promoting tumorigenesis across various cancer types, its specific role in LUAD remains underexplored. This study aims to elucidate the molecular mechanisms by which NCAPD2 contributes to LUAD progression, with a focus on its involvement in the AKTMDM2/E2F1 positive feedback loop. MATERIALS AND

methodsNCAPD2 expression in LUAD and normal tissues was analyzed using Western blotting and immunohistochemistry (IHC). Functional assays, including colony formation, wound healing, Transwell assays, and in vivo mouse models were conducted to evaluate the impact of NCAPD2 on LUAD cell proliferation, invasion, and metastasis. RNA sequencing and protein interaction experiments were used to investigate the role of NCAPD2 in the PI3K/AKT/MDM2 pathway and its interaction with E2F1.

resultsThis study first identified that NCAPD2 expression is significantly upregulated in LUAD tissues, particularly in higher pathological stages. NCAPD2 overexpression promoted LUAD cell proliferation and metastasis, while its knockdown inhibited tumor growth and invasion. Mechanistically, NCAPD2 activated the PI3K/Akt pathway, facilitating the interaction between MDM2 and E2F1, reducing E2F1 ubiquitination, and increasing its expression. Furthermore, E2F1 enhanced NCAPD2 transcription, forming a positive feedback loop that drives LUAD progression.

conclusionThis study reveals a novel role of NCAPD2 in promoting LUAD progression through the AKT/MDM2/E2F1 positive feedback loop. These findings provide new insights into the molecular pathogenesis of LUAD and suggest NCAPD2 as a potential therapeutic target for improving patient outcomes.

Indexed as

Adaptor Proteins, Signal TransducingAdenocarcinoma of LungE2F1 Transcription FactorLung NeoplasmsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mdm2AnimalsCell Line, TumorCell ProliferationDisease ProgressionFeedback, PhysiologicalFemaleGene Expression Regulation, NeoplasticHumansMaleMiceAdaptor Proteins, Signal TransducingE2F1 protein, humanE2F1 Transcription FactorMDM2 protein, humanProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mdm2E2F1Lung adenocarcinomaNCAPD2PI3K/AKT/MDM2 pathwaypositive feedback loop

Identifiers

PMID41319185
PMCPMC12676955

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.