Evidence map›Paper›PMID 31876369›Full record

ArticleMolecular oncology2020

SNX16 activates c-Myc signaling by inhibiting ubiquitin-mediated proteasomal degradation of eEF1A2 in colorectal cancer development.

Zhiyong Shen, Yongsheng Li, Yuan Fang, Mingdao Lin, Xiaochuang Feng, Zhenkang Li, Yizhi Zhan, Yuechen Liu, Tingyu Mou, Xiaoliang Lan and 4 more

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 36 citations in OpenAlex.

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  10. Significant position of C-myc in colorectal cancer: a promising therapeutic target.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    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

14 authors at 2 institutions in 2 countries.

Zhiyong ShenDepartment of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yongsheng LiDepartment of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.ORCID 0000-0002-6069-0862
Yuan FangDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Mingdao LinDepartment of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Xiaochuang FengDepartment of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Zhenkang LiDepartment of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yizhi ZhanDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yuechen LiuDepartment of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Tingyu MouDepartment of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Xiaoliang LanDepartment of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yanan WangDepartment of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Guoxin LiDepartment of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jiping WangDivision of Surgical Oncology, Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Haijun DengDepartment of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.ORCID 0000-0003-4632-2702
Nanfang Hospital · CNBrigham and Women's Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sorting nexin 16 (SNX16), a member of the sorting nexin family, has been implicated in tumor development. However, the function of SNX16 has not yet been investigated in colorectal cancer (CRC). Here, we showed that SNX16 expression was significantly upregulated in CRC tissues compared with normal counterparts. Upregulated mRNA levels of SNX16 predicted poor survival of CRC patients. Functional experiments showed that SNX16 could promote CRC cells growth both in vitro and in vivo. Knockdown of SNX16 induced cell cycle arrest and apoptosis, whereas ectopic overexpression of SNX16 had the opposite effects. Mechanistically, SNX16-eukaryotic translation elongation factor 1A2 (eEF1A2) interaction could inhibit the degradation and ubiquitination of eEF1A2, followed by activation of downstream c-Myc signaling. Our study unveiled that the SNX16/eEF1A2/c-Myc signaling axis could promote colorectal tumorigenesis and SNX16 might potentially serve as a novel biomarker for the diagnosis and an intervention of CRC.

Indexed as

AgedAnimalsApoptosisCarcinogenesisCell Cycle CheckpointsCell Line, TumorCell ProliferationColorectal NeoplasmsFemaleHumansImmunohistochemistryMaleMass SpectrometryMiceMice, NudeMiddle AgedEEF1A2 protein, humanPeptide Elongation Factor 1Proteasome Endopeptidase ComplexProto-Oncogene Proteins c-mycSNX16 protein, humanSorting NexinsUbiquitincell proliferationc-Myccolorectal cancereEF1A2SNX16

Identifiers

PMID31876369
PMCPMC6998659
OpenAlexW2996843328

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.