Evidence map›Paper›PMID 38302412›Full record

ArticleCell death & disease2024

FSTL3 promotes tumor immune evasion and attenuates response to anti-PD1 therapy by stabilizing c-Myc in colorectal cancer.

Haiyang Li, Na Zheng, Anning Guo, Weiwei Tang, Muxin Li, Yuanyuan Cao, Xinhua Ma, Hongyong Cao, Yong Ma, Hanjin Wang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 15 citations in OpenAlex.

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  11. Targeting tumor metabolism to augment CD8Journal of pharmaceutical analysis · 2025
    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

11 authors at 3 institutions in 1 country.

Haiyang LiDepartment of general surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Na ZhengGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Anning GuoGeneral Clinical Research Center, Nanjing First Hospital, China Pharmaceutical University, Nanjing, Jiangsu, China.
Weiwei TangHepatobiliary/Liver Transplantation Center, the First Affiliated Hospital of Nanjing Medical University, Key Laboratory of Living Donor Transplantation, Chinese Academy of Medical Sciences, Nanjing, Jiangsu, China.ORCID 0000-0002-8516-819X
Muxin LiGeneral Clinical Research Center, Nanjing First Hospital, China Pharmaceutical University, Nanjing, Jiangsu, China.
Yuanyuan CaoGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Xinhua MaGeneral Clinical Research Center, Nanjing First Hospital, China Pharmaceutical University, Nanjing, Jiangsu, China.
Hongyong CaoDepartment of general surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China. caohongy6167@163.com.ORCID 0000-0003-1188-991X
Yong MaDepartment of general surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China. yma0917@163.com.
Hanjin WangDepartment of general surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China. whj_888@sohu.com.
Shuli ZhaoGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China. shulizhao79@163.com.ORCID 0000-0002-3610-2418
China Pharmaceutical University · CNNanjing Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81872114National Natural Science Foundation of China (National Science Foundation of China) 82173205
6 · The paper itself

Abstract

Programmed cell death 1 ligand 1 (PDL1)/programmed cell death 1 (PD1) blockade immunotherapy provides a prospective strategy for the treatment of colorectal cancer (CRC), but various constraints on the effectiveness of the treatment are still remaining. As reported in previous studies, follistatin-like 3 (FSTL3) could mediate inflammatory response in macrophages by induction lipid accumulation. Herein, we revealed that FSTL3 were overexpressed in malignant cells in the CRC microenvironment, notably, the expression level of FSTL3 was related to tumor immune evasion and the clinical efficacy of anti-PD1 therapy. Further studies determined that hypoxic tumor microenvironment induced the FSTL3 expression via HIF1α in CRC cells, FSTL3 could bind to the transcription factor c-Myc (354-406 amino acids) to suppress the latter's ubiquitination and increase its stability, thereby to up-regulated the expression of PDL1 and indoleamine 2,3-dioxygenase 1 (IDO1). The results in the immunocompetent tumor models verified that FSLT3 knockout in tumor cells increased the proportion of CD8

Indexed as

CD8-Positive T-LymphocytesColorectal NeoplasmsHumansImmunotherapyT-Lymphocytes, RegulatoryTumor EscapeTumor Microenvironment

Identifiers

PMID38302412
PMCPMC10834545
OpenAlexW4391449327

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.