Evidence map›Paper›PMID 40858654›Full record

ArticleScientific reports2025

Hypoxia suppressed the Siglec-5 signaling in TAMs via modulating the balance of SHP2/SYK activation in hepatocellular carcinoma.

ShuBin Luo, JiaXi Mao, Lei Zhang, JiaJing Duan, GuoYou Xue, Qian Xu, ETao Yu

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. Article
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.

ShuBin Luo *Department of General Surgery (Section 1), The First People's Hospital of Jinghong, Xishuangbanna Dai Autonomous Prefecture, Yunnan Province, China.
JiaXi Mao *Department of Liver Surgery and Organ Transplantation, Changzheng Hospital, Naval Medical University, Shanghai, 200003, China.
Lei Zhang *Department of General Surgery, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 20001, China.
JiaJing DuanDepartment of General Surgery (Section 1), The First People's Hospital of Jinghong, Xishuangbanna Dai Autonomous Prefecture, Yunnan Province, China.
GuoYou XueDepartment of General Surgery (Section 1), The First People's Hospital of Jinghong, Xishuangbanna Dai Autonomous Prefecture, Yunnan Province, China.
Qian XuThe People's Hospital of Xishuangbanna Dai Autonomous Prefecture Medical Laboratory, 4 Gai Lan Nan Road, Jinghong Street, Jinghong City, Xishuangbanna Dai Autonomous Prefecture, 666100, Yunnan Province, China. 18306915669@163.com.
ETao YuThe People's Hospital of Xishuangbanna Dai Autonomous Prefecture Medical Laboratory, 4 Gai Lan Nan Road, Jinghong Street, Jinghong City, Xishuangbanna Dai Autonomous Prefecture, 666100, Yunnan Province, China. 764557640@qq.com.

Funding

Basic medical research project of Naval Medical University 2022QN072Open Research Project Program of the State Key Laboratory of Medical Immunology NKLMI2023K03
6 · The paper itself

Abstract

objectiveTo investigate the effects of Siglec-5 on hepatocellular carcinoma and the mechanism of action. The interactions and expression changes between Siglec-5 and Siglec-14 not only affect immune cell function, but may also influence tumor progression. A deeper understanding of the mechanisms regulating their balance could provide new insights and strategies for hepatocellular carcinoma treatment.

methodsA cell co-culture model was established. Western blotting was used to detect protein expression in different groups. The CCK-8 assay was employed to observe the proliferation of HepG2 hepatocellular carcinoma cells, and the Transwell assay was used to examine their migration. Tumorigenic capacity of HepG2 cells detected by subcutaneous transplantation tumor assay in nude mice.

resultsOverexpression of Siglec-5 under hypoxic conditions resulted in increased levels of SHP2 and arginase-1 proteins and decreased levels of P-SYK, IL-1β, and TNFα proteins. Addition of SHP2 inhibitor under hypoxic conditions or Siglec-5 overexpression resulted in increased expression of P-SYK and NOX4 proteins and decreased levels of arginase-1. When Siglec-5 expression was inhibited under hypoxic conditions, the levels of P-SHP2 and arginase-1 were decreased, whereas the levels of P-SYK, IL-1β, and TNFα were increased. The expression of P-SYK, NOX4, IL-1β, and TNFα was decreased, whereas the levels of arginase-1 were increased after the use of SYK inhibitors under hypoxic conditions that inhibited Siglec-5 expression. The proliferation, migration and tumorigenicity of HepG2 cells were increased when Siglec-5 was overexpressed under hypoxic conditions, while the proliferation, migration and tumorigenicity of HepG2 cells were decreased when Siglec-5 was inhibited under hypoxic conditions.

conclusionHypoxia suppressed the Siglec-5 signaling in TAMs via modulating the balance of SHP2/SYK activation in hepatocellular carcinoma.

Indexed as

Antigens, CDAntigens, Differentiation, B-LymphocyteAntigens, Differentiation, MyelomonocyticCarcinoma, HepatocellularHypoxiaLiver NeoplasmsProtein Tyrosine Phosphatase, Non-Receptor Type 11Syk KinaseTumor-Associated MacrophagesAnimalsCell HypoxiaCell MovementCell ProliferationHep G2 CellsHumansMiceAntigens, CDAntigens, Differentiation, B-LymphocyteAntigens, Differentiation, MyelomonocyticProtein Tyrosine Phosphatase, Non-Receptor Type 11PTPN11 protein, humanSyk KinaseSYK protein, humanHepatocellular carcinomaROSSHP2/SYKSiglec-5

Identifiers

PMID40858654
PMCPMC12381118

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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.