Evidence map›Paper›PMID 36688997›Full record

ArticleCancer immunology, immunotherapy : CII2023

LINC01004-SPI1 axis-activated SIGLEC9 in tumor-associated macrophages induces radioresistance and the formation of immunosuppressive tumor microenvironment in esophageal squamous cell carcinoma.

Fen Zhao, Hui Tian, Yungang Wang, Jianbo Zhang, Fang Liu, Lei Fu

Open access · hybridAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
14.0field-weighted citation impact, top 1% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

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  5. The Role of Mucins in Esophageal Inflammatory Diseases.Journal of personalized medicine · 2026
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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

6 authors at 3 institutions in 1 country.

Fen Zhao *Department of Radiation Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, 250117, Shandong, People's Republic of China.
Hui Tian *Department of Radiation Oncology, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, People's Republic of China.
Yungang Wang *Department of Radiation Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, 250117, Shandong, People's Republic of China.
Jianbo ZhangDepartments of Pathology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, 250117, Shandong, People's Republic of China.
Fang LiuDepartment of Imaging, Shandong Medical College, Jinan, 250002, Shandong, People's Republic of China.
Lei FuDepartment of Radiation Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, 250117, Shandong, People's Republic of China. fuiray08@163.com.
Shandong Tumor Hospital · CNShandong First Medical University · CNQilu Hospital of Shandong University · CN

Funding

Beijing Xisike Clinical Oncology Research Foundation, CSCO-Leading Oncology Research Fund Y-2019AZQN-0036Natural Science Foundation of Shandong Province, Joint Fund for Cancer Prevention and Treatment (Key Support Projects) ZR2020LZL013
6 · The paper itself

Abstract

Radioresistance and immunosuppression remain the major obstacles in the anti-cancer treatments. This work studies the functions of sialic acid binding Ig like lectin 9 (SIGLEC9) and its related molecules in radioresistance and immunosuppression in esophageal squamous cell carcinoma (ESCC). The single-cell analysis showed that SIGLEC9 was mainly expressed on tumor-associated macrophages (TAMs). Monocytes-derived macrophages were co-cultured with ESCC cells and subjected to radiotherapy. High or low doses of radiotherapy induced SIGLEC9 upregulation and M2 polarization of TAMs. Artificial inhibition of SIGLEC9 in TAMs suppressed the radioresistance and immunosuppressive tumor microenvironment (TME) in the co-cultured ESCC cells. Upstream molecules of SIGLEC9 were predicted via bioinformatics. LINC01004 recruited Spi-1 proto-oncogene (SPI1) in nucleus of TAMs to induce transcriptional activation of SIGLEC9. SIGLEC9 interacted with mucin 1 (MUC1). MUC1 overexpression in ESCCs induced M2 skewing of TAMs, enhanced radioresistance and immunosuppression, and promoted nuclear translocation of β-catenin to suppress radiotherapy-induced ferroptosis of ESCC cells. These effects were blocked upon SIGLEC9 suppression. In vitro results were reproduced in the animal models with xenograft tumors. Taken together, this study demonstrates that the LINC01004-SPI1 axis-activated SIGLEC9 in TAMs induces radioresistance and the formation of immunosuppressive TME in ESCC.

Indexed as

Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaAnimalsAntigens, CDCell Line, TumorHumansProto-Oncogene Protein Spi-1RNA, Long NoncodingSialic Acid Binding Immunoglobulin-like LectinsTumor-Associated MacrophagesTumor MicroenvironmentAntigens, CDProto-Oncogene Protein Spi-1RNA, Long NoncodingSialic Acid Binding Immunoglobulin-like LectinsSIGLEC9 protein, humanEsophageal squamous cell carcinomaMUC1RadioresistanceSIGLEC9Tumor-associated macrophages

Identifiers

PMID36688997
PMCPMC10198857
OpenAlexW4317777174

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.