Evidence map›Paper›PMID 40610622›Full record

ArticleCellular and molecular life sciences : CMLS2025

Aquaglyceroporin-7 ameliorates sorafenib resistance and immune evasion in hepatocellular carcinoma through inhibition of lipid accumulation.

Guangsi He, Wenzhu Shao, Weifei Wang, Lu Sun, Beibei Gao, Jie Wei

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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

6 authors.

Guangsi HeOncology Department 2, The Affiliated Chuzhou Hospital of Anhui Medical University, Chuzhou, 239001, Anhui, P.R. China.
Wenzhu ShaoOncology Department 1, The Affiliated Chuzhou Hospital of Anhui Medical University, No. 12, Zhongyou Lane, Gulou Street, Langya District, Chuzhou, 239001, Anhui, P.R. China.
Weifei WangOncology Department 2, The Affiliated Chuzhou Hospital of Anhui Medical University, Chuzhou, 239001, Anhui, P.R. China.
Lu SunOncology Department 1, The Affiliated Chuzhou Hospital of Anhui Medical University, No. 12, Zhongyou Lane, Gulou Street, Langya District, Chuzhou, 239001, Anhui, P.R. China.
Beibei GaoNursing Department, The Affiliated Chuzhou Hospital of Anhui Medical University, Chuzhou, 239001, Anhui, P.R. China.
Jie WeiOncology Department 1, The Affiliated Chuzhou Hospital of Anhui Medical University, No. 12, Zhongyou Lane, Gulou Street, Langya District, Chuzhou, 239001, Anhui, P.R. China. w_j_doc1222@163.com.ORCID http://orcid.org/0009-0006-9979-4470

Funding

Higher Education Science Research Project of Anhui Province (Natural Science Category) 2023AH050669
6 · The paper itself

Abstract

Sorafenib, a multikinase inhibitor targeting cell growth and angiogenesis, was approved for advanced unresectable hepatocellular carcinoma (HCC) in 2007. This investigation aims to elucidate the involvement of aquaglyceroporin-7 (AQP7) in regulating sorafenib resistance (SR) in HCC. AQP7 was downregulated in HCC-SR cells. AQP7 upregulation inhibited lipid accumulation, enhanced the sorafenib sensitivity of SR cells, and improved immune evasion. TBX19 protein was elevated in HCC-SR cells, and TBX19 repressed AQP7 transcription by binding to its promoter. E3-ubiquitin ligase MGRN1 was reduced in HCC, and its overexpression promoted TBX19 degradation. MGRN1 overexpression enhanced AQP7 and improved SR and immune evasion in HCC, which was reversed by TBX19 overexpression. Mouse HCC cells Hepa1-6 were used to construct an orthotopic tumor model and to analyze the effects of AQP7 and MGRN1 expression on the in vivo antitumor effects of Sorafenib, lipid accumulation in tumor tissues, and immune cell infiltration. MGRN1 silencing in Hepa1-6 cells induced sorafenib resistance and created an immunosuppressive tumor microenvironment, which was repressed by AQP7 upregulation. In conclusion, MGRN1 loss in HCC-SR cells blocked TBX19 degradation and strengthened TBX19-mediated AQP7 repression, leading to immune evasion. Targeting this signaling might offer a promising therapeutic strategy to overcome SR in HCC.

Indexed as

AquaporinsCarcinoma, HepatocellularDrug Resistance, NeoplasmImmune EvasionLipid MetabolismLiver NeoplasmsSorafenibAnimalsAntineoplastic AgentsCell Line, TumorGene Expression Regulation, NeoplasticHumansMaleMiceMice, Inbred BALB CMice, NudeAntineoplastic AgentsAquaporinsSorafenibT-Box Domain ProteinsUbiquitin-Protein LigasesChemoresistanceOrthotopic tumorsTranscription factorTumor microenvironmentUbiquitination

Identifiers

PMID40610622
PMCPMC12229415

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Registered trials

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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.