Evidence map›Paper›PMID 36631249›Full record

ArticleGut2023

S100A10 promotes HCC development and progression via transfer in extracellular vesicles and regulating their protein cargos.

Xia Wang, Hongyang Huang, Karen Man-Fong Sze, Jin Wang, Lu Tian, Jingyi Lu, Yu-Man Tsui, Hoi Tang Ma, Eva Lee, Ao Chen and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Gut, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
12.5field-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

32 citing papers in PubMed, 49 citations in OpenAlex.

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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

16 authors at 4 institutions in 2 countries.

Xia WangDepartment of Pathology, University of Hong Kong Faculty of Medicine, Hong Kong, Hong Kong.
Hongyang HuangDepartment of Pathology, University of Hong Kong Faculty of Medicine, Hong Kong, Hong Kong.
Karen Man-Fong SzeDepartment of Pathology, University of Hong Kong Faculty of Medicine, Hong Kong, Hong Kong.
Jin WangLiaoning University, Shenyang, Liaoning, China.
Lu TianDepartment of Pathology, University of Hong Kong Faculty of Medicine, Hong Kong, Hong Kong.
Jingyi LuDepartment of Pathology, University of Hong Kong Faculty of Medicine, Hong Kong, Hong Kong.
Yu-Man TsuiDepartment of Pathology, University of Hong Kong Faculty of Medicine, Hong Kong, Hong Kong.
Hoi Tang MaDepartment of Pathology, University of Hong Kong Faculty of Medicine, Hong Kong, Hong Kong.
Eva LeeDepartment of Pathology, University of Hong Kong Faculty of Medicine, Hong Kong, Hong Kong.
Ao ChenDepartment of Pathology, University of Hong Kong Faculty of Medicine, Hong Kong, Hong Kong.
Joyce LeeDepartment of Pathology, University of Hong Kong Faculty of Medicine, Hong Kong, Hong Kong.
Ying WangSun Yat-Sen University Cancer Center, Guangzhou, Guangdong, China.
Judy Wai Ping YamDepartment of Pathology, University of Hong Kong Faculty of Medicine, Hong Kong, Hong Kong.ORCID 0000-0002-5637-121X
Tan-To CheungState Key Laboratory of Liver Research, The University of Hong Kong, Hong Kong, Hong Kong.
Xinyuan GuanState Key Laboratory of Liver Research, The University of Hong Kong, Hong Kong, Hong Kong.ORCID 0000-0002-4485-6017
Irene Oi-Lin NgDepartment of Pathology, University of Hong Kong Faculty of Medicine, Hong Kong, Hong Kong iolng@hku.hk.ORCID 0000-0001-7532-2029
University of Hong Kong · HKChinese University of Hong Kong · HKLiaoning University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveGrowing evidence indicates that tumour cells exhibit characteristics similar to their lineage progenitor cells. We found that S100 calcium binding protein A10 (S100A10) exhibited an expression pattern similar to that of liver progenitor genes. However, the role of S100A10 in hepatocellular carcinoma (HCC) progression is unclear. Furthermore, extracellular vesicles (EVs) are critical mediators of tumourigenesis and metastasis, but the extracellular functions of S100A10, particularly those related to EVs (EV-S100A10), are unknown.

designThe functions and mechanisms of S100A10 and EV-S100A10 in HCC progression were investigated in vitro and in vivo. Neutralising antibody (NA) to S100A10 was used to evaluate the significance of EV-S100A10.

resultsFunctionally, S100A10 promoted HCC initiation, self-renewal, chemoresistance and metastasis in vitro and in vivo. Of significance, we found that S100A10 was secreted by HCC cells into EVs both in vitro and in the plasma of patients with HCC. S100A10-enriched EVs enhanced the stemness and metastatic ability of HCC cells, upregulated epidermal growth factor receptor (EGFR), AKT and ERK signalling, and promoted epithelial-mesenchymal transition. EV-S100A10 also functioned as a chemoattractant in HCC cell motility. Of significance, S100A10 governed the protein cargos in EVs and mediated the binding of MMP2, fibronectin and EGF to EV membranes through physical binding with integrin αⅤ. Importantly, blockage of EV-S100A10 with S100A10-NA significantly abrogated these enhancing effects.

conclusionAltogether, our results uncovered that S100A10 promotes HCC progression significantly via its transfer in EVs and regulating the protein cargoes of EVs. EV-S100A10 may be a potential therapeutic target and biomarker for HCC progression.

Indexed as

Carcinoma, HepatocellularExtracellular VesiclesLiver NeoplasmsCell CommunicationCell Line, TumorHumansHEPATOCELLULAR CARCINOMAMOLECULAR MECHANISMSMOLECULAR ONCOLOGY

Identifiers

PMID36631249
PMCPMC10314046
OpenAlexW4315641430

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.