Evidence map›Paper›PMID 35459781›Full record

ArticleOncogene2022

Galectin-1 orchestrates an inflammatory tumor-stroma crosstalk in hepatoma by enhancing TNFR1 protein stability and signaling in carcinoma-associated fibroblasts.

Yao-Tsung Tsai, Chih-Yi Li, Yen-Hua Huang, Te-Sheng Chang, Chung-Yen Lin, Chia-Hsien Chuang, Chih-Yang Wang, Gangga Anuraga, Tzu-Hao Chang, Tsung-Chieh Shih and 10 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.5field-weighted citation impact, top 10% of its field
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

22 citing papers in PubMed, 31 citations in OpenAlex.

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  17. Cancer-Associated Fibroblasts in Hepatocellular Carcinoma and Cholangiocarcinoma.Cellular and molecular gastroenterology and hepatology · 2023
    Review
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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

20 authors at 8 institutions in 3 countries.

Yao-Tsung Tsai *International PhD Program for Translational Science, Taipei Medical University, Taipei, Taiwan.
Chih-Yi Li *International PhD Program for Translational Science, Taipei Medical University, Taipei, Taiwan.
Yen-Hua HuangGraduate Institute of Translational Medicine, College of Medical Sciences and Technology, Taipei Medical University, Taipei, Taiwan.ORCID http://orcid.org/0000-0001-6020-9998
Te-Sheng ChangCollege of Medicine, Chang Gung University, Taoyuan, Taiwan.
Chung-Yen LinInstitute of Information Science, Academia Sinica, Taipei, Taiwan.ORCID http://orcid.org/0000-0002-4733-9488
Chia-Hsien ChuangInstitute of Information Science, Academia Sinica, Taipei, Taiwan.ORCID http://orcid.org/0000-0002-3639-4684
Chih-Yang WangGraduate Institute of Cancer Biology and Drug Discovery, Taipei Medical University, Taipei, Taiwan.ORCID http://orcid.org/0000-0002-4137-5074
Gangga AnuragaGraduate Institute of Cancer Biology and Drug Discovery, Taipei Medical University, Taipei, Taiwan.
Tzu-Hao ChangGraduate Institute of Biomedical Informatics, College of Medical Sciences and Technology, Taipei Medical University, Taipei, Taiwan.ORCID http://orcid.org/0000-0001-7011-3754
Tsung-Chieh ShihDepartment of Biochemistry and Molecular Medicine, University of California, Davis, Sacramento, CA, USA.ORCID http://orcid.org/0000-0001-7992-1504
Zu-Yau LinHepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.
Yuh-Ling ChenInstitute of Oral Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan.ORCID http://orcid.org/0000-0001-7760-5954
Ivy ChungUniversiti Malaya Cancer Research Institute, Faculty of Medicine, Universiti Malaya, Kuala Lumpur, 50603, Malaysia.ORCID http://orcid.org/0000-0003-2840-8123
Kuen-Haur LeeGraduate Institute of Cancer Biology and Drug Discovery, Taipei Medical University, Taipei, Taiwan.
Che-Chang ChangInternational PhD Program for Translational Science, Taipei Medical University, Taipei, Taiwan.ORCID http://orcid.org/0000-0001-8080-2094
Shian-Ying SungInternational PhD Program for Translational Science, Taipei Medical University, Taipei, Taiwan.
Kai-Huei YangInternational PhD Program for Translational Science, Taipei Medical University, Taipei, Taiwan.
Wan-Lin TsuiInternational PhD Program for Translational Science, Taipei Medical University, Taipei, Taiwan.
Chee-Voon YapInternational PhD Program for Translational Science, Taipei Medical University, Taipei, Taiwan.
Ming-Heng WuInternational PhD Program for Translational Science, Taipei Medical University, Taipei, Taiwan. mhwu1015@tmu.edu.tw.ORCID http://orcid.org/0000-0002-5740-9144
Taipei Medical University · TWChang Gung University · TWInstitute of Information Science, Academia Sinica · TWKaohsiung Medical University · TWNational Cheng Kung University · TWTakming University of Science and Technology · TWUniversity of California, Davis · USUniversity of Malaya · MY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Most cases of hepatocellular carcinoma (HCC) arise with the fibrotic microenvironment where hepatic stellate cells (HSCs) and carcinoma-associated fibroblasts (CAFs) are critical components in HCC progression. Therefore, CAF normalization could be a feasible therapy for HCC. Galectin-1 (Gal-1), a β-galactoside-binding lectin, is critical for HSC activation and liver fibrosis. However, few studies has evaluated the pathological role of Gal-1 in HCC stroma and its role in hepatic CAF is unclear. Here we showed that Gal-1 mainly expressed in HCC stroma, but not cancer cells. High expression of Gal-1 is correlated with CAF markers and poor prognoses of HCC patients. In co-culture systems, targeting Gal-1 in CAFs or HSCs, using small hairpin (sh)RNAs or an therapeutic inhibitor (LLS30), downregulated plasminogen activator inhibitor-2 (PAI-2) production which suppressed cancer stem-like cell properties and invasion ability of HCC in a paracrine manner. The Gal-1-targeting effect was mediated by increased a disintegrin and metalloprotease 17 (ADAM17)-dependent TNF-receptor 1 (TNFR1) shedding/cleavage which inhibited the TNF-α → JNK → c-Jun/ATF2 signaling axis of pro-inflammatory gene transcription. Silencing Gal-1 in CAFs inhibited CAF-augmented HCC progression and reprogrammed the CAF-mediated inflammatory responses in a co-injection xenograft model. Taken together, the findings uncover a crucial role of Gal-1 in CAFs that orchestrates an inflammatory CSC niche supporting HCC progression and demonstrate that targeting Gal-1 could be a potential therapy for fibrosis-related HCC.

Indexed as

Cancer-Associated FibroblastsCarcinoma, HepatocellularLiver NeoplasmsCell Line, TumorFibroblastsGalectin 1HumansProtein StabilityReceptors, Tumor Necrosis Factor, Type ITumor MicroenvironmentGalectin 1Receptors, Tumor Necrosis Factor, Type I

Identifiers

PMID35459781
OpenAlexW4224274635

What Socratic holds

Textmetadata
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 Socratic graph.