Evidence map›Paper›PMID 39873845›Full record

ArticleCell biology and toxicology2025

HSP27/IL-6 axis promotes OSCC chemoresistance, invasion and migration by orchestrating macrophages via a positive feedback loop.

Ying Qi, Juan Cao, Mingjing Jiang, Ying Lin, Weibo Li, Bo Li

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell biology and toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

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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.

Ying Qi *Department of Oral Anatomy and Physiology, Hospital of Stomatology, Jilin Provincial Key Laboratory of Oral Biomedical Engineering, Jilin University, Changchun, 130021, China.
Juan Cao *Department of Oral Anatomy and Physiology, Hospital of Stomatology, Jilin Provincial Key Laboratory of Oral Biomedical Engineering, Jilin University, Changchun, 130021, China.
Mingjing JiangDepartment of Oral Anatomy and Physiology, Hospital of Stomatology, Jilin Provincial Key Laboratory of Oral Biomedical Engineering, Jilin University, Changchun, 130021, China.
Ying LinDepartment of Oral Anatomy and Physiology, Hospital of Stomatology, Jilin Provincial Key Laboratory of Oral Biomedical Engineering, Jilin University, Changchun, 130021, China.
Weibo LiDepartment of Oral Anatomy and Physiology, Hospital of Stomatology, Jilin Provincial Key Laboratory of Oral Biomedical Engineering, Jilin University, Changchun, 130021, China.
Bo LiDepartment of Oral Anatomy and Physiology, Hospital of Stomatology, Jilin Provincial Key Laboratory of Oral Biomedical Engineering, Jilin University, Changchun, 130021, China. lbo@jlu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Novel strategies to disrupt tumor progression have emerged from studying the interactions between tumor cells and tumor-associated macrophages (TAMs). However, the molecular mechanisms of interactions between tumor cells and TAMs underlying oral squamous cell carcinoma (OSCC) progression have not been fully elucidated. This study explored the molecular mechanism of the HSP27/IL-6 axis in OSCC chemoresistance, invasion, and migration. Here, we demonstrated the higher expression of HSP27 in OSCC cells. Paracrine HSP27 from OSCC cells enhanced chemoresistance, invasion, migration, and EMT in OSCC by inducing M2 polarization and IL-6 secretion in TAMs. HSP27 and IL-6 established a positive feedback loop between OSCC cells and M2 TAMs. TAMs-derived IL-6 orchestrated OSCC stemness and chemoresistance through upregulating β-catenin and CD44, and enhanced OSCC invasion, migration, and EMT via autocrine HSP27/TLR4 signaling. Collectively, HSP27/IL-6 axis facilitates OSCC chemoresistance, invasion, and migration by orchestrating macrophages through a positive feedback loop. We identify the regulatory mechanism underlying the interaction and crosstalk between OSCC cells and TAMs mediated by the HSP27/IL-6 axis. Targeting the HSP27/IL-6 axis could be a promising treatment strategy for OSCC patients, potentially controlling disease progression and improving prognosis and recurrence outcomes.

Indexed as

Carcinoma, Squamous CellDrug Resistance, NeoplasmHSP27 Heat-Shock ProteinsInterleukin-6MacrophagesMouth NeoplasmsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionFeedback, PhysiologicalHeat-Shock ProteinsHumansMolecular ChaperonesNeoplasm InvasivenessSignal TransductionTumor-Associated MacrophagesHeat-Shock ProteinsHSP27 Heat-Shock ProteinsHSPB1 protein, humanIL6 protein, humanInterleukin-6Molecular ChaperonesChemoresistanceHSP27IL-6MacrophagesOral squamous cell carcinomaTLR4

Identifiers

PMID39873845
PMCPMC11775009

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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 OpenQuestion graph.