Evidence map›Paper›PMID 41496407›Full record

ArticleTranslational oncology2026

Interleukin 35 promotes progression of hepatocellular carcinoma by recruiting neutrophils.

Wei Gan, Guo-Qiang Sun, Jin-Long Huang, Bao-Ye Sun, Zhu-Tao Wang, Zhang-Fu Yang, Cheng Zhou, Yong Yi, Shuang-Jian Qiu

Abstract read
In one paragraph

Article in Translational oncology, 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.

Wei GanDepartment of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Guo-Qiang SunDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Liver Cancer Institute, Fudan University, Key Laboratory for Carcinogenesis & Cancer Invasion, The Chinese Ministry of Education, Shanghai, PR China.
Jin-Long HuangDepartment of neurosurgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Bao-Ye SunDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Liver Cancer Institute, Fudan University, Key Laboratory for Carcinogenesis & Cancer Invasion, The Chinese Ministry of Education, Shanghai, PR China.
Zhu-Tao WangDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Liver Cancer Institute, Fudan University, Key Laboratory for Carcinogenesis & Cancer Invasion, The Chinese Ministry of Education, Shanghai, PR China.
Zhang-Fu YangDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Liver Cancer Institute, Fudan University, Key Laboratory for Carcinogenesis & Cancer Invasion, The Chinese Ministry of Education, Shanghai, PR China.
Cheng ZhouDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Liver Cancer Institute, Fudan University, Key Laboratory for Carcinogenesis & Cancer Invasion, The Chinese Ministry of Education, Shanghai, PR China.
Yong YiDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Liver Cancer Institute, Fudan University, Key Laboratory for Carcinogenesis & Cancer Invasion, The Chinese Ministry of Education, Shanghai, PR China. Electronic address: yi.yong@zs-hospital.sh.cn.
Shuang-Jian QiuDepartment of Liver Surgery and Transplantation, Zhongshan Hospital, Fudan University, Liver Cancer Institute, Fudan University, Key Laboratory for Carcinogenesis & Cancer Invasion, The Chinese Ministry of Education, Shanghai, PR China. Electronic address: qiu.shuangjian@zs-hospital.sh.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundA growing number of therapeutic strategies against hepatocellular carcinoma (HCC) have emerged. However, their efficacy remains limited. This study investigated the mechanism of interleukin-35 (IL-35) in the progression of HCC and its potential application in HCC treatment.

methodsThe expression of IL-35,Gp130 ,IL12-Rβ2, CCL3,etc. in HCC tissues was detected by immunohistochemistry(IHC), and the expression of IL-35 in HCC cell lines was detected by fluorescence assay. Kaplan-Meier survival analysis of IL-35 and its receptor in relation to overall survival(OS) and recurrence free survival(RFS) in patients with HCC. The mouse subcutaneous tumor models to study the effects of IL-35 on HCC growth and immune cells. Western blot were used to detect the expression IL-35, CCL3, FGF2, and flow cytometric plot were performed to explore the immune cells infiltration in the tumor tissue.

resultsHigh expression of IL-35 in patients with HCC was associated with poor prognosis. Furthermore, IL-35 could facilitate tumor progression by affecting neutrophil infiltration, angiogenesis, and CD8+ T-cell infiltration. Additionally, CCL3 was a key factor mediating the recruitment of neutrophils by IL-35. FGF2 derived from neutrophils stimulated by IL-35 promoted intratumoral angiogenesis. IL-35 also facilitated the adhesion of tumors to endothelial cells, with neutrophils further enhancing this effect both. Anti-IL-35 antibody combined with anti-PD1 antibody significantly enhanced which therapeutic effect in HCC.

conclusionsOur data show that the high expression of IL-35 in patients with HCC is an important tumor promoter. Combined treatment with anti-IL-35 and anti-PD1 antibodies have potential therapeutic effect against HCC.

Indexed as

Anti-PD1Hepatocellular carcinomaImmunotherapyInterleukin 35Neutrophil

Identifiers

PMID41496407
PMCPMC12813232

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.