Evidence map›Paper›PMID 42465011›Full record

ArticleAmerican journal of cancer research2026

Serum amyloid P component suppresses melanoma growth and metastasis by inhibiting CCL1 secretion from macrophages.

Pei Tang, Ying Wang, Bo Zhao, Bohan Zheng, Bin Li, Shuang Wu, Xiaoming Li, Lijing Wang, Cuiling Qi

Abstract read
In one paragraph

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

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Pei TangLaboratory of Oncology and Immunology, School of Basic Medical Sciences, Guangdong Pharmaceutical University Guangzhou 510006, Guangdong, China.
Ying WangLaboratory of Oncology and Immunology, School of Basic Medical Sciences, Guangdong Pharmaceutical University Guangzhou 510006, Guangdong, China.
Bo ZhaoDepartment of Rehabilitation, The First Affiliated Hospital, Jinan University Guangzhou 510632, Guangdong, China.
Bohan ZhengLaboratory of Oncology and Immunology, School of Basic Medical Sciences, Guangdong Pharmaceutical University Guangzhou 510006, Guangdong, China.
Bin LiLaboratory of Oncology and Immunology, School of Basic Medical Sciences, Guangdong Pharmaceutical University Guangzhou 510006, Guangdong, China.
Shuang WuLaboratory of Oncology and Immunology, School of Basic Medical Sciences, Guangdong Pharmaceutical University Guangzhou 510006, Guangdong, China.
Xiaoming LiLaboratory of Oncology and Immunology, School of Basic Medical Sciences, Guangdong Pharmaceutical University Guangzhou 510006, Guangdong, China.
Lijing WangLaboratory of Oncology and Immunology, School of Basic Medical Sciences, Guangdong Pharmaceutical University Guangzhou 510006, Guangdong, China.
Cuiling QiLaboratory of Oncology and Immunology, School of Basic Medical Sciences, Guangdong Pharmaceutical University Guangzhou 510006, Guangdong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The incidence of melanoma, which is among the most common skin cancers, has significantly increased at an alarming rate over the past decade. Serum amyloid P component (SAP), a member of the pentraxin (PTX) family, is a major acute-phase protein in mice. The effects of SAP on melanoma and the mechanisms underlying these effects remain unclear. In the current study, we established xenograft and metastatic melanoma models in SAP-overexpressing (SAP-Tg) mice to determine the effect of SAP on the progression of melanoma. Compared with wild-type (WT) mice, SAP-Tg mice developed tumors with smaller volumes and fewer metastatic foci, and the degree of cell proliferation within the transplanted tumors was significantly decreased by SAP. Further study indicated that SAP inhibited melanoma growth and metastasis by suppressing CC-chemokine 1 (CCL1) secretion from activated macrophages, while CCL1 promoted the migration and invasion of B16F10 melanoma cells. Furthermore, SAP-induced CCL1 downregulation suppressed Ras/p-ERK pathway activation. These findings indicate a new effect of SAP mediated via a novel mechanism and provide direct evidence that SAP may have therapeutic value for melanoma.

Indexed as

CCL1macrophagemelanomamelanoma growthmelanoma metastasisSAP

Identifiers

PMID42465011
PMCPMC13373559

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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.