Evidence map›Paper›PMID 41203580›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Smoking-Induced STC2

Yujie Shen, Lianchong Gao, Qiang Huang, Liang Zhou, Chengzhi Xu, Chunping Wu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Smoking-Induced STC2Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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

6 authors.

Yujie ShenDepartment of Otolaryngology, Shanghai Key Clinical Disciplines of otorhinolaryngology, Eye Ear Nose & Throat Hospital, Fudan University, Shanghai, 200025, P. R. China.
Lianchong GaoShanghai Center for Systems Biomedicine, Key Laboratory of Systems Biomedicine (Ministry of Education), Shanghai JiaoTong University, Shanghai, 200025, P. R. China.
Qiang HuangDepartment of Otolaryngology, Shanghai Key Clinical Disciplines of otorhinolaryngology, Eye Ear Nose & Throat Hospital, Fudan University, Shanghai, 200025, P. R. China.
Liang ZhouDepartment of Otolaryngology, Shanghai Key Clinical Disciplines of otorhinolaryngology, Eye Ear Nose & Throat Hospital, Fudan University, Shanghai, 200025, P. R. China.
Chengzhi XuDepartment of Otolaryngology, Shanghai Key Clinical Disciplines of otorhinolaryngology, Eye Ear Nose & Throat Hospital, Fudan University, Shanghai, 200025, P. R. China.
Chunping WuDepartment of Otolaryngology, Shanghai Key Clinical Disciplines of otorhinolaryngology, Eye Ear Nose & Throat Hospital, Fudan University, Shanghai, 200025, P. R. China.ORCID https://orcid.org/0000-0002-0712-8715

Funding

Minimally Invasive Endoscopic Surgery Center for Head & Neck Tumor, EENT Hospital of Fudan University ZBZX033National Natural Science Foundation of China 82372972National Natural Science Foundation of China 82401339 82403387Science and Technology Development Fund of Shanghai Pudong New Area PKJ2024-Y02Shanghai Anticancer Association EYAS PROJECT SACA-CY24B06Shanghai Sailing Program 23YF1404700Special Fund for Clinical Research in Health Industry of Shanghai Municipal Commission of Health 202240320
6 · The paper itself

Abstract

Smoking-associated laryngeal squamous cell carcinoma (LSCC) is characterized by high metastatic potential and poor prognosis. However, the underlying molecular mechanisms remain insufficiently understood. This study utilized single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics to explore the heterogeneity of the tumor microenvironment in smoking-associated LSCC. Thirteen distinct cellular subpopulations within the tumor microenvironment are identified, with STC2 and ITGA5 emerging as smoking-associated prognostic markers. STC2 exhibited bifurcated differentiation within tumor epithelial cells, categorized as Tumor_C1 and Tumor_C2. The two subtypes are linked to vascular permeability and DNA replication pathways, respectively. Mechanistically, nicotine activated the JAK2/STAT3 signaling pathway through CHRNA5, resulting in direct STAT3 binding to the STC2 promoter and modulation of its transcription. STC2 subsequently upregulated TGFBI, which interacted with ITGA5 on endothelial cells, regulating vascular permeability and facilitating hematogenous dissemination of LSCC cells. Furthermore, STC2 knockdown altered F-actin cytoskeletal dynamics by modulating small GTPase signaling, impairing filopodia formation and epithelial polarity restoration. This study elucidates the tumor-endothelial interactions mediated by STC2 and ITGA5 in smoking-associated LSCC, emphasizing their roles in tumor progression and vascular permeability. These findings suggest potential prognostic biomarkers and therapeutic targets to improve the clinical management of smoking-associated LSCC.

Indexed as

Carcinoma, Squamous CellIntercellular Signaling Peptides and ProteinsLaryngeal NeoplasmsSmokingSquamous Cell Carcinoma of Head and NeckCell Line, TumorGene Expression Regulation, NeoplasticHumansSignal TransductionSingle-Cell AnalysisTranscriptomeTumor MicroenvironmentIntercellular Signaling Peptides and Proteinslaryngeal squamous cell carcinomasingle‐cell RNA sequencingsmokingspatial transcriptomicstumor microenvironment

Identifiers

PMID41203580
PMCPMC12849985

What OpenQuestion holds

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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.