Evidence map›Paper›PMID 34023852›Full record

ArticleCell death & disease2021

DPP3/CDK1 contributes to the progression of colorectal cancer through regulating cell proliferation, cell apoptosis, and cell migration.

Yixin Tong, Yuan Huang, Yuchao Zhang, Xiangtai Zeng, Mei Yan, Zhongsheng Xia, Dongming Lai

Erratum issuedOpen 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. An erratum has been issued. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.1field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 48 citations in OpenAlex.

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  18. A Mini-review onEndocrine, metabolic & immune disorders drug targets · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 5 institutions in 1 country.

Yixin Tong *Department of Tongji Medical College of Huazhong University, 1095 Jiefang Dadao, Wuhan, Hubei Province, China.
Yuan Huang *Department of Endoscopy Center, Zhongshan Hospital of Fudan University, 180 Fenglin Road, Xuhui, Shanghai, China.
Yuchao Zhang *Department of Gastrointestinal Surgery, Sun Yat-sen memorial Hospital of Sun Yat-sen University, 107 Yanjiang West Road, Guangzhou, Guangdong Province, China.
Xiangtai ZengDepartment of The First Affiliated Hospital, Gannan Medical University, 23 Qingnian Road, Zhanggong District, Ganzhou, Jiangxi Province, China.
Mei YanDepartment of Gastrointestinal Surgery, Sun Yat-sen memorial Hospital of Sun Yat-sen University, 107 Yanjiang West Road, Guangzhou, Guangdong Province, China.
Zhongsheng XiaDepartment of Gastrointestinal Surgery, Sun Yat-sen memorial Hospital of Sun Yat-sen University, 107 Yanjiang West Road, Guangzhou, Guangdong Province, China. xiazhsh@163.com.
Dongming LaiDepartment of Gastrointestinal Surgery, Sun Yat-sen memorial Hospital of Sun Yat-sen University, 107 Yanjiang West Road, Guangzhou, Guangdong Province, China. laidm@mail.sysu.edu.cn.
Sun Yat-sen University · CNFudan University · CNGannan Medical University · CNHuazhong University of Science and Technology · CNSun Yat-sen Memorial Hospital · CN

Funding

Guangdong Science and Technology Department (Science and Technology Department, Guangdong Province) No. 2012B031800377
6 · The paper itself

Abstract

At present, colorectal cancer (CRC) has become a serious threat to human health in the world. Dipeptidyl peptidase 3 (DPP3) is a zinc-dependent hydrolase that may be involved in several physiological processes. However, whether DPP3 affects the development and progression of CRC remains a mystery. This study is the first to demonstrate the role of DPP3 in CRC. Firstly, the results of immunohistochemistry analysis showed the upregulation of DPP3 in CRC tissues compared with normal tissues, which is statistically analyzed to be positively correlated with lymphatic metastasis, pathological stage, positive number of lymph nodes. Moreover, the high expression of DPP3 predicts poor prognosis in CRC patients. In addition, the results of cell dysfunction experiments clarified that the downregulation of DPP3 significantly inhibited cell proliferation, colony formation, cell migration, and promoted apoptosis in vitro. DPP3 depletion could induce cell apoptosis by upregulating the expression of BID, BIM, Caspase3, Caspase8, HSP60, p21, p27, p53, and SMAC. In addition, downregulation of DPP3 can reduce tumorigenicity of CRC cells in vivo. Furthermore, CDK1 is determined to be a downstream target of DPP3-mediated regulation of CRC by RNA-seq, qPCR, and WB. The interaction between DPP3 and CDK1 shows mutual regulation. Specifically, downregulation of DPP3 can accentuate the effects of CDK1 knockdown on the function of CRC cells. Overexpression of CDK1 alleviates the inhibitory effects of DPP3 knockdown in CRC cells. In summary, DPP3 has oncogene-like functions in the development and progression of CRC by targeting CDK1, which may be an effective molecular target for the prognosis and treatment of CRC.

Indexed as

AdultAgedAged, 80 and overAnimalsApoptosisCase-Control StudiesCDC2 Protein KinaseCell MovementCell ProliferationColorectal NeoplasmsDipeptidyl-Peptidases and Tripeptidyl-PeptidasesDisease ProgressionFemaleGene Expression Regulation, NeoplasticHCT116 CellsHumansCDC2 Protein KinaseCDK1 protein, humanDipeptidyl-Peptidases and Tripeptidyl-PeptidasesDPP3 protein, humanRNA, Small Interfering

Identifiers

PMID34023852
PMCPMC8141054
OpenAlexW3164638850

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.