Evidence map›Paper›PMID 30250219›Full record

ArticleCell death & disease2018

POFUT1 promotes colorectal cancer development through the activation of Notch1 signaling.

Yuheng Du, Daojiang Li, Nanpeng Li, Chen Su, Chunxing Yang, Changwei Lin, Miao Chen, Runliu Wu, Xiaorong Li, Gui Hu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.3field-weighted citation impact, top 11% 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, 56 citations in OpenAlex.

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  15. Preliminary study on the mechanism of POFUT1 in colorectal cancer.Medical oncology (Northwood, London, England) · 2023
    Article
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  18. Review
  19. Journal of Cancer · 2022
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  20. American journal of cancer research · 2022
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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 2 institutions in 1 country.

Yuheng DuDepartment of Gastrointestinal Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan Province, China.
Daojiang LiDepartment of Gastrointestinal Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan Province, China.
Nanpeng LiDepartment of Gastrointestinal Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan Province, China.
Chen SuDepartment of Gastrointestinal Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan Province, China.
Chunxing YangDepartment of Gastrointestinal Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan Province, China.
Changwei LinDepartment of Gastrointestinal Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan Province, China.
Miao ChenDepartment of Gastrointestinal Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan Province, China.
Runliu WuDepartment of Gastrointestinal Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan Province, China.
Xiaorong LiDepartment of Gastrointestinal Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan Province, China.
Gui HuDepartment of Gastrointestinal Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan Province, China. hugui22@qq.com.
Third Xiangya Hospital · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Copy number variations (CNVs) are key drivers of colorectal cancer (CRC). Our previous studies revealed that protein O-fucosyltransferase 1 (POFUT1) overexpression is driven by CNVs during CRC development. The potential role and underlying mechanisms of POFUT1 in CRC were not investigated. In this study, we analyzed the expression of POFUT1 in CRC from cosmic and TCGA databases and confirmed that POFUT1 is highly expressed in CRC. We used well characterized CRC cell lines, including SW620 and HCT116 to establish a model POFUT1 knockdown cell line. Using these cells, we investigated the role of POFUT1 in CRC. Our data revealed that silencing POFUT1 in CRC cells inhibits cell proliferation, decreases cell invasion and migration, arrests cell cycle progression, and stimulates CRC cell apoptosis in vitro. We further demonstrate that POFUT1 silencing dramatically suppresses CRC tumor growth and transplantation in vivo. We additionally reveal new mechanistic insights into the role of POFUT1 during CRC, through demonstrating that POFUT1 silencing inhibits Notch1 signaling. Taken together, our findings demonstrate that POFUT1 is a tumor activating gene during CRC development, which positively regulates CRC tumor progression through activating Notch1.

Indexed as

AnimalsApoptosisCarcinogenesisCell Cycle CheckpointsCell MovementCell ProliferationColorectal NeoplasmsDatabases, GeneticFucosyltransferasesGene Knockdown TechniquesHCT116 CellsHumansMiceMice, NudeModels, AnimalNeoplasm InvasivenessFucosyltransferasesNOTCH1 protein, humanpolypeptide fucosyltransferaseReceptor, Notch1

Identifiers

PMID30250219
PMCPMC6155199
OpenAlexW2892066994

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.