Evidence map›Paper›PMID 42059013›Full record

ArticleJournal of hepatocellular carcinoma2026

SEMA4F Regulates the Malignant Phenotype of Hepatocellular Carcinoma Cells Through the PI3K-Akt Pathway.

Jing-Jing Wang, Lei Xie, Xiang Wang, Xing-Yu Chen, Xiao Xu, Ping-Ping Zhai, Zhi-Zheng Xu, Kai Chen

Abstract read
In one paragraph

Article in Journal of hepatocellular carcinoma, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Jing-Jing WangDepartment of Oncology, The First Affiliated Hospital of Soochow University, Suzhou, 215006, People's Republic of China.
Lei XieDepartment of Oncology, Taizhou Hospital of Traditional Chinese Medicine, Taizhou, 225300, People's Republic of China.
Xiang WangDepartment of Oncology, Taizhou Hospital of Traditional Chinese Medicine, Taizhou, 225300, People's Republic of China.
Xing-Yu ChenDepartment of General Surgery, Taizhou Fourth People's Hospital, Taizhou, 225300, People's Republic of China.
Xiao XuDepartment of Oncology, Taizhou Hospital of Traditional Chinese Medicine, Taizhou, 225300, People's Republic of China.
Ping-Ping ZhaiDepartment of Oncology, Taizhou Hospital of Traditional Chinese Medicine, Taizhou, 225300, People's Republic of China.ORCID 0009-0009-1879-0470
Zhi-Zheng XuDepartment of Oncology, Changxing People's Hospital, Huzhou, 313100, People's Republic of China.
Kai ChenDepartment of Oncology, The First Affiliated Hospital of Soochow University, Suzhou, 215006, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Hepatocellular carcinoma (HCC) is the most common pathological type of liver cancer. SEMA4F is an immune-related gene associated with HCC survival. As a transmembrane semaphorin, semaphorin 4F plays a key role in various biological processes. Recent studies have found that semaphorin 4F is closely related to cancer progression, but its role in HCC remains unclear. In this study, we aimed to investigate the function and related mechanisms of SEMA4F in HCC. Methods: Public databases were used to analyze the expression and prognosis of SEMA4F in HCC. Overexpression/knockdown cell models were constructed via lentiviral transfection/siRNA technology. The function of SEMA4F was explored through in vitro cellular experiments. Transcriptome sequencing was employed to investigate its molecular mechanisms, and Western blot was used to validate the expression of pathway proteins. Results: SEMA4F expression was elevated in tumor tissues of HCC patients and was associated with poor prognosis and shorter overall survival. In vitro analyses showed that SEMA4F overexpression promoted the proliferation, invasion, and migration of HCC cells, while SEMA4F knockdown led to the opposite phenotype. Furthermore, SEMA4F partially promoted HCC cell proliferation, migration, and invasion by activating the PI3K-Akt pathway; inhibition of this pathway significantly attenuated the pro‑proliferative, migratory, and invasive effects of SEMA4F. Conclusion: Our study reveals the function of SEMA4F in HCC. These findings suggest that SEMA4F is a potential prognostic biomarker for HCC and exerts pro‑cancer effects through activation of the PI3K-Akt pathway. These findings suggest SEMA4F as a potential therapeutic target, pending in vivo validation and clinical investigation.

Indexed as

hepatocellular carcinomaHUH-7PI3K-Akt pathwayPLCSEMA4F

Identifiers

PMID42059013
PMCPMC13123568

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