Evidence map›Paper›PMID 35210436›Full record

ArticleCell death & disease2022

M1 macrophage-derived exosomes and their key molecule lncRNA HOTTIP suppress head and neck squamous cell carcinoma progression by upregulating the TLR5/NF-κB pathway.

Huaili Jiang, Lei Zhou, Na Shen, Xianhui Ning, Daquan Wu, Kanglun Jiang, Xinsheng Huang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
9.6field-weighted citation impact, top 1% of its field
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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 115 citations in OpenAlex.

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  9. The role of exosomal long non-coding RNAs in head, neck and thyroid cancers.Medical oncology (Northwood, London, England) · 2025
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10 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Huaili JiangDepartment of Otolaryngology, Zhongshan Hospital, Fudan University, Shanghai, China.
Lei ZhouDepartment of Otolaryngology, Zhongshan Hospital, Fudan University, Shanghai, China.
Na ShenDepartment of Otolaryngology, Zhongshan Hospital, Fudan University, Shanghai, China.
Xianhui NingDepartment of Otolaryngology, Zhongshan Hospital, Fudan University, Shanghai, China.
Daquan WuDepartment of Otolaryngology, Zhongshan Hospital, Fudan University, Shanghai, China.
Kanglun JiangDepartment of Otolaryngology, Zhongshan Hospital, Fudan University, Shanghai, China.
Xinsheng HuangDepartment of Otolaryngology, Zhongshan Hospital, Fudan University, Shanghai, China. huang.xinsheng@zs-hospital.sh.cn.ORCID http://orcid.org/0000-0003-3201-4776
Sun Yat-sen University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exosomes serve as a crucial mode of communication between tumor-associated macrophages (TAMs) and cancer cells. This study attempted to explore the function of M1-derived exosomes and clarify their specific mechanism in head and neck squamous cell carcinoma (HNSCC). Moreover, the functional roles of M1-derived exosomes and their key molecule long noncoding RNA (lncRNA) HOXA transcript at the distal tip (HOTTIP) in HNSCC were investigated by conducting a series of in vitro and in vivo experiments. The dual-luciferase test was utilized to clarify the binding capacities between HOTTIP/mRNA and miRNAs. Accordingly, HOTTIP was found to be upregulated in M1-derived exosomes. Meanwhile, the in vitro experiments indicated that M1 exosomes suppressed proliferation, migration and invasion but induced apoptosis of cancer cells. This function was noted to be enhanced by HOTTIP-overexpressed M1 exosomes but was weakened by HOTTIP-knockdown ones, indicating that HOTTIP serves as a key molecule in M1 exosomes. Therefore, the function of HOTTIP in cancer cells was explored, for which overexpression of HOTTIP was found to inhibit proliferation, migration and invasion but induced apoptosis of cancer cells in vitro. A mechanism study further showed that M1 exosomes and HOTTIP activated the TLR5/NF-κB signaling pathway by competitively sponging miR-19a-3p and miR-19b-3p. Furthermore, cancer cells expressing HOTTIP were noted to induce the polarization of both local M1 and M2 macrophages; however, M1 exosomes were observed to reprogram local TAMs into M1 macrophages. More importantly, both cancer cells expressing HOTTIP and M1 exosomes reeducated circulating monocytes to express the M1 phenotype. The corresponding data demonstrated that the M1 exosomal lncRNA HOTTIP suppresses HNSCC progression by upregulating the TLR5/NF-κB signaling pathway through competitively sponging miR-19a-3p and miR-19b-3p. In particular, M1 exosomes and HOTTIP induce the polarization of M1 in circulating monocytes, thus providing novel insight into HNSCC immunotherapy.

Indexed as

ExosomesHead and Neck NeoplasmsMicroRNAsRNA, Long NoncodingSquamous Cell Carcinoma of Head and NeckCell ProliferationHumansMacrophagesNF-kappa BToll-Like Receptor 5long noncoding RNA HOTTIP, humanMicroRNAsMIRN19A microRNA, humanNF-kappa BRNA, Long NoncodingTLR5 protein, humanToll-Like Receptor 5

Identifiers

PMID35210436
PMCPMC8873565
OpenAlexW4213432709

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.