Evidence map›Paper›PMID 34452648›Full record

ArticleCell & bioscience2021

A novel mechanism for C1GALT1 in the regulation of gastric cancer progression.

Xiaoxia Dong, Chunli Chen, Xinzhou Deng, Yongyu Liu, Qiwen Duan, Zhen Peng, Zhiguo Luo, Li Shen

Abstract read
In one paragraph

Article in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

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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

8 authors.

Xiaoxia Dong *Department of Clinical Oncology, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.
Chunli Chen *Department of Clinical Oncology, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.
Xinzhou DengDepartment of Clinical Oncology, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.
Yongyu LiuDepartment of Clinical Oncology, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.
Qiwen DuanDepartment of Clinical Oncology, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.
Zhen PengDepartment of Clinical Oncology, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.
Zhiguo LuoDepartment of Clinical Oncology, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China. zhiguo_luo@163.com.
Li ShenDepartment of Clinical Oncology, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China. 20101061@hbmu.edu.cn.ORCID http://orcid.org/0000-0002-7348-4718

Funding

National Natural Science Foundation of China 81902494
6 · The paper itself

Abstract

backgroundGastric cancer (GC) is a highly aggressive and lethal disease around the world. High expression of core 1 β 1, 3-galactosyltransferase 1 (C1GALT1), the primary enzyme responsible for protein O-glycosylation, plays a critical role in gastric carcinogenesis. However, proteins that can be O-glycosylated by C1GALT1 in GC have not been completely elucidated. Also, the mechanism leading to its upregulation in GC is currently unknown.

resultsUsing public databases and our patient samples, we confirmed that C1GALT1 expression was upregulated at both the mRNA and protein levels in GC tissues. Elevated expression of C1GALT1 protein was closely associated with advanced TNM stage, lymph node metastasis, tumor recurrence, and poor overall survival. With gain- and loss-of-function approaches, we demonstrated that C1GALT1 promoted GC cell proliferation, migration, and invasion. By employing lectin pull-down assay and mass spectrometry, integrin α5 was identified as a new downstream target of C1GALT1 in GC. C1GALT1 was able to modify O-linked glycosylation on integrin α5 and thereby modulate the activation of the PI3K/AKT pathway. Functional experiments indicated that integrin α5 inhibition could reverse C1GALT1-mediated tumor growth and metastasis both in vitro and in vivo. Moreover, transcription factor SP1 was found to bind to the C1GALT1 promoter region and activated its expression. Further investigation proved that miR-152 negatively regulated C1GALT1 expression by directly binding to its 3' -UTR.

conclusionsOur findings uncover a novel mechanism for C1GALT1 in the regulation of GC progression. Thus, C1GALT1 may serve as a promising target for the diagnosis and treatment of GC.

Indexed as

C1GALT1Gastric cancerGlycosyltransferaseMalignant progression

Identifiers

PMID34452648
PMCPMC8393437

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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.