Evidence map›Paper›PMID 40366858›Full record

ArticleCancer biology & therapy2025

Silencing ZIC5 suppresses glycolysis and promotes disulfidptosis in lung adenocarcinoma cells.

Cimei Zeng, Denggao Huang, Lei Wang, Haimei Liang, Ximiao Ma

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PubMed Full text at PMC Publisher
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Article in Cancer biology & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

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0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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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

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3 · Its place in the literature

Who cites it

14 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Cimei ZengDepartment of Respiratory and Critical Care Medicine, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, Hainan, China.ORCID 0009-0008-4467-5372
Denggao HuangCentral Laboratory, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, Hainan, China.
Lei WangDepartment of Respiratory and Critical Care Medicine, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, Hainan, China.
Haimei LiangDepartment of Respiratory and Critical Care Medicine, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, Hainan, China.
Ximiao MaThoracic Surgery, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, Hainan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis study aims to explore the effects of silencing Zic family member 5 (ZIC5) on glucose metabolism and disulfidptosis in lung adenocarcinoma (LUAD) cells.

methodsData from The Cancer Genome Atlas (TCGA) was used to analyze ZIC5 expression in LUAD and its association with patient outcomes. ZIC5 was silenced in A549 and H1299 cells using siRNA. The expression of ZIC5 mRNA and protein was assessed by qRT-PCR and Western blot. Cell proliferation was evaluated through CCK-8 and 5-ethynyl-2'-deoxyuridine (EdU) assays, while glucose uptake, lactate production, and ATP levels were measured to assess energy metabolism. Seahorse XF analysis was used to evaluate extracellular acidification rate (ECAR) and oxygen consumption rate (OCR). Disulfidptosis was assessed through NADP

resultsZIC5 is highly expressed in LUAD and is associated with poor patient prognosis. Silencing ZIC5 significantly reduced its mRNA and protein levels in A549 and H1299 cells, markedly inhibited cell proliferation, and led to significant decreases in glucose uptake, lactate production, ATP levels, ECAR, and OCR. Additionally, silencing ZIC5 resulted in an increased NADP

conclusionZIC5 plays a crucial role in promoting LUAD cell proliferation and energy metabolism while inhibiting disulfidptosis. Silencing ZIC5 markedly suppresses these processes, indicating its potential as a therapeutic target in LUAD.

Indexed as

Adenocarcinoma of LungGlycolysisLung NeoplasmsTranscription FactorsApoptosisCell Line, TumorCell ProliferationDisulfidptosisGene Expression Regulation, NeoplasticGene SilencingHumansPrognosisTranscription Factorsdisulfidptosisglucose metabolismglycolysisLung adenocarcinomaZIC5

Identifiers

PMID40366858
PMCPMC12080275

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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.