Evidence map›Paper›PMID 30541550›Full record

ArticleMolecular cancer2018

TRIB2 functions as novel oncogene in colorectal cancer by blocking cellular senescence through AP4/p21 signaling.

Zhenlin Hou, Kaixuan Guo, Xuling Sun, Fuqing Hu, Qianzhi Chen, Xuelai Luo, Guihua Wang, Junbo Hu, Li Sun

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

54 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
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  4. The role of tribbles homolog 2 in cell proliferation.Cell communication and signaling : CCS · 2025
    Review
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  14. International journal of molecular sciences · 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

9 authors at 2 institutions in 1 country.

Zhenlin HouCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
Kaixuan GuoCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
Xuling SunCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
Fuqing HuCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
Qianzhi ChenCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
Xuelai LuoCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
Guihua WangCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
Junbo HuCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
Li SunDepartment of Oncology, Tongji Hospital, Huazhong University of Science and Technology, 1095 Jiefang Av, Wuhan, Hubei, 430030, People's Republic of China. litchisun@163.com.
Tongji Hospital · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCellular senescence is a state of irreversible cell growth arrest and senescence cells permanently lose proliferation potential. Induction of cellular senescence might be a novel therapy for cancer cells. TRIB2 has been reported to participate in regulating proliferation and drug resistance of various cancer cells. However, the role of TRIB2 in cellular senescence of colorectal cancer (CRC) and its molecular mechanism remains unclear.

methodsThe expression of TRIB2 in colorectal cancer tissues and adjacent tissues was detected by immunohistochemistry and RT-PCR. The growth, cell cycle distribution and cellular senescence of colorectal cancer cells were evaluated by Cell Counting Kit-8 (CCK8) assay, flow cytometry detection and senescence-associated β-galactosidase staining, respectively. Western blot, RT-PCR and luciferase assay were performed to determine how TRIB2 regulates p21. Immunoprecipitation (IP) and chromatin-immunoprecipitation (ChIP) were used to investigate the molecular mechanisms.

resultsWe found that TRIB2 expression was elevated in CRC tissues compared to normal adjacent tissues and high TRIB2 expression indicated poor prognosis of CRC patients. Functionally, depletion of TRIB2 inhibited cancer cells proliferation, induced cell cycle arrest and promoted cellular senescence, whereas overexpression of TRIB2 accelerated cell growth, cell cycle progression and blocked cellular senescence. Further studies showed that TRIB2 physically interacted with AP4 and inhibited p21 expression through enhancing transcription activities of AP4. The rescue experiments indicated that silencing of AP4 abrogated the inhibition of cellular senescence induced by TRIB2 overexpression.

conclusionThese data demonstrate that TRIB2 suppresses cellular senescence through interaction with AP4 to down-regulate p21 expression. Therefore, TRIB2 could be a potential target for CRC treatment.

Indexed as

Basic Helix-Loop-Helix Leucine Zipper Transcription FactorsCalcium-Calmodulin-Dependent Protein KinasesCell CycleCell Cycle CheckpointsCell LineCell ProliferationCellular SenescenceColorectal NeoplasmsCyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsHEK293 CellsHumansIntracellular Signaling Peptides and ProteinsOncogenesRNA-Binding ProteinsSignal TransductionBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCalcium-Calmodulin-Dependent Protein KinasesCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsIntracellular Signaling Peptides and ProteinsREPIN1 protein, humanRNA-Binding ProteinsTRIB2 protein, humanAP4Cellular senescenceColorectal cancerp21p53TRIB2

Identifiers

PMID30541550
PMCPMC6291992
OpenAlexW2904862932

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.