Evidence map›Paper›PMID 34702807›Full record

ArticleCell death & disease2021

The overexpression of Tipe2 in CRC cells suppresses survival while endogenous Tipe2 accelerates AOM/DSS induced-tumor initiation.

Yan Li, Na Zhang, Chao Ma, Wenwen Xu, Guiyuan Jin, Yi Zheng, Lei Zhang, Bingyu Liu, Chengjiang Gao, Suxia Liu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
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  4. TIPE2 deficiency amplifies inflammation and immune dysregulation in MASH through modulating hepatic lipid metabolism and immune cell function.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  6. 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

10 authors at 1 institution in 1 country.

Yan LiKey Laboratory of Infection and Immunity of Shandong Province, Department of Immunology, Shandong University School of Basic Medical Science, Jinan, Shandong, China.
Na ZhangKey Laboratory of Infection and Immunity of Shandong Province, Department of Immunology, Shandong University School of Basic Medical Science, Jinan, Shandong, China.
Chao MaDepartment of Pathology, Shandong University School of Basic Medical Science, Ji'nan, People's Republic of China.
Wenwen XuKey Laboratory of Infection and Immunity of Shandong Province, Department of Immunology, Shandong University School of Basic Medical Science, Jinan, Shandong, China.
Guiyuan JinKey Laboratory of Infection and Immunity of Shandong Province, Department of Immunology, Shandong University School of Basic Medical Science, Jinan, Shandong, China.
Yi ZhengKey Laboratory of Infection and Immunity of Shandong Province, Department of Immunology, Shandong University School of Basic Medical Science, Jinan, Shandong, China.
Lei ZhangKey Laboratory of Infection and Immunity of Shandong Province, Department of Immunology, Shandong University School of Basic Medical Science, Jinan, Shandong, China.
Bingyu LiuKey Laboratory of Infection and Immunity of Shandong Province, Department of Immunology, Shandong University School of Basic Medical Science, Jinan, Shandong, China.
Chengjiang GaoKey Laboratory of Infection and Immunity of Shandong Province, Department of Immunology, Shandong University School of Basic Medical Science, Jinan, Shandong, China.ORCID 0000-0002-9365-4497
Suxia LiuKey Laboratory of Infection and Immunity of Shandong Province, Department of Immunology, Shandong University School of Basic Medical Science, Jinan, Shandong, China. suxiasd@163.com.ORCID 0000-0003-3537-0274
Shandong University · CN

Funding

National Outstanding Youth Foundation of China 81525012National Science Foundation of China | National Natural Science Foundation of China-Yunnan Joint Fund (NSFC-Yunnan Joint Fund) 81873864
6 · The paper itself

Abstract

Aging is a natural and progressive process characterized by an increased frequency of age-related diseases such as cancer. But its mechanism is unclear. TNFAIP8L2 (Tipe2) is an important negative regulator for homeostasis through inhibiting TLR and TCR signaling. Our work reveals that Tipe2 might have dual function by regulating senescence. One side, the overexpression of Tipe2 in CRC cells could induce typical senescent phenotype, especially exposure to oxidative stress. Tipe2 inhibits telomerase activity by regulating c-Myc and c-Est-2 binding to the hTERT promotor. Interestingly, Tipe2 KO mice treated with D-Gal showed a less serious inverse of CD4:CD8 ratio, a lower percentage of Treg compared to WT. Besides, Tipe2 KO mice were more tolerant to the initiation of AOM/DSS-induced CRC, accompanied by a lower level of Treg within IEL. Therefore, specific antibodies against CD25 effectively ameliorate tumorigenesis. These data suggest strongly that the overexpressed Tipe2 suppresses tumor cells proliferation and survival, but endogenous Tipe2 promotes the initiation of tumorigenesis when exposure to dangerous environment such as AOM/DSS-related inflammation.

Indexed as

AnimalsCell Line, TumorCell ProliferationCell Transformation, NeoplasticDisease Models, AnimalHumansIntracellular Signaling Peptides and ProteinsMiceSignal TransductionIntracellular Signaling Peptides and ProteinsTIPE2 protein, mouse

Identifiers

PMID34702807
PMCPMC8548391
OpenAlexW3210119302

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.