Evidence map›Paper›PMID 42351282›Full record

ArticleHereditas2026

M2 macrophage-derived exosomes promote the malignant progression and glycolysis of cervical cancer via Msi1.

Liting Sun, Abudureyimu Tunishahan, Xiaowen Li

Abstract read
In one paragraph

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

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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Liting SunDepartment of Gynecological Malignancy Radiotherapy, The Affiliated cancer Hospital of Xinjiang Medical University, Urumqi City, Xinjiang, 830011, China.
Abudureyimu TunishahanDepartment of Gynecological Malignancy Radiotherapy, The Affiliated cancer Hospital of Xinjiang Medical University, Urumqi City, Xinjiang, 830011, China.
Xiaowen LiDepartment of Gynecological Malignancy Radiotherapy, The Affiliated cancer Hospital of Xinjiang Medical University, Urumqi City, Xinjiang, 830011, China. lixiaowen1026@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCervical cancer is a common gynecologic malignancy characterized by high recurrence and metastasis rate. Exosomes derived from M2-polarized tumor-associated macrophages play a key role in promoting tumorigenesis and cancer progression. Additionally, musashi1 (Msi1) is a key oncoprotein across multiple malignancies. Therefore, this study aims to determine the role of M2 macrophage-derived exosomal Msi1 in cervical cancer progression and glycolysis and to clarify the underlying mechanism.

methodsM2 macrophages were identified using microscope, flow cytometry, and western blot. Gene mRNA and protein expression levels were analyzed via quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. The cell proliferation, invasion, apoptosis, and sphere formation were assessed using 5-Ethynyl-2'-deoxyuridine (EdU) staining, Transwell, flow cytometry, and sphere formation assay, respectively. The glucose uptake and lactate production were determined using commercial kits. Exosomes were identified using western blot, transmission electron microscopy, and nanoparticle tracking analysis (NTA). Cellular uptake of exosomes was assessed by incubating SiHa and Ca Ski cells with PKH67-labeled exosomes. Cervical cancer xenograft mouse models were established to analyze the role of M2 macrophage-derived exosomal Msi1.

resultsMsi1 expression was increased in M2 macrophages (**P < 0.01 and ***P < 0.001). Functionally, M2 macrophages enhanced cervical cancer cell proliferation, invasion, aerobic glycolysis, and stemness as well as suppressed cell apoptosis through secreting exosomes (*P < 0.05, **P < 0.01, and ***P < 0.001). Importantly, Msi1 expression was increased in M2 macrophage-derived exosomes (***P < 0.001). Mechanically, M2 macrophage-derived exosomes promoted malignancy and glycolysis by carrying Msi1 (*P < 0.01 and ***P < 0.001). In vivo, M2 macrophage-derived exosomal Msi1 accelerated cervical cancer progression (***P < 0.001).

conclusionM2 macrophage-derived exosomes promote cervical cancer progression and glycolysis by delivering Msi1 to recipient cells.

Indexed as

ExosomesGlycolysisMacrophagesNerve Tissue ProteinsRNA-Binding ProteinsUterine Cervical NeoplasmsAnimalsApoptosisCell Line, TumorCell ProliferationDisease ProgressionFemaleHumansMiceMSI1 protein, humanNerve Tissue ProteinsRNA-Binding ProteinsCervical cancerExosomesGlycolysisM2 macrophagesMusashi1

Identifiers

PMID42351282
PMCPMC13678903

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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.