Evidence map›Paper›PMID 32105413›Full record

ArticleJournal of cellular and molecular medicine2020

SEZ6L2 knockdown impairs tumour growth by promoting caspase-dependent apoptosis in colorectal cancer.

Ning An, Yaqin Zhao, Haitao Lan, Ming Zhang, Yuan Yin, Cheng Yi

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

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  6. Overexpression of SEZ6L2 and Immune Infiltration in Cancer Based on Gene Image Diagnosis.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024
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  13. High expression ofGland surgery · 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

6 authors at 3 institutions in 1 country.

Ning AnDepartment of Abdominal Cancer, West China Hospital, West China Clinical Medical School, Sichuan University, Chengdu, China.
Yaqin ZhaoDepartment of Abdominal Cancer, West China Hospital, West China Clinical Medical School, Sichuan University, Chengdu, China.
Haitao LanCancer Center, Academy of Medical Sciences and Sichuan Provincial People's Hospital, Affiliated Hospital of University of Electronic Science and Technology of China, Chengdu, China.
Ming ZhangCancer Center, Academy of Medical Sciences and Sichuan Provincial People's Hospital, Affiliated Hospital of University of Electronic Science and Technology of China, Chengdu, China.
Yuan YinDepartment of Gastrointestinal Surgery, West China Hospital and State Key Laboratory of Biotherapy, Sichuan University, Chengdu, China.
Cheng YiDepartment of Abdominal Cancer, West China Hospital, West China Clinical Medical School, Sichuan University, Chengdu, China.ORCID 0000-0001-7306-7263
University of Electronic Science and Technology of China · CNWest China Medical Center of Sichuan University · CNSichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Seizure-related 6 homolog (mouse)-like 2 (SEZ6L2) was shown to be involved in transcription of a type 1 transmembrane protein for regulating cell fate. Until now, the expression and function of SEZ6L2 in various cancers, including colorectal cancer (CRC), were unclear. In the present study, we determined the expression of SEZ6L2 in a tissue microarray from patients with CRC and then, analysed the correlation between SEZ6L2 expression and the prognosis of the patients. Furthermore, the potential function of SEZ6L2 in CRC was determined using cell counting kit, colony formation assay and xenograft model in vitro and in vivo. Flow cytometry, Western blotting, immunohistochemical staining and a blocking experiment were employed to investigate the underlying mechanism of SEZ6L2 regulating CRC growth. Our results indicated that SEZ6L2 was significantly up-regulated in tumour tissues of patients with CRC compared with adjacent normal tissues. Up-regulation of SEZ6L2 was correlated with a poor prognosis in patients with CRC. In vitro experiments suggested that the knockdown of SEZ6L2 inhibits CRC cell growth and colony formation, but it has no significant impact on the invasion. The antitumour effects of shSEZ6L2 were also confirmed by a xenograft model. Investigations of the mechanisms indicated that the knockdown of SEZ6L2 impairs the growth of the CRC cells by inducing caspase-dependent apoptosis, which was mediated by mitochondria-related proteins. Furthermore, SEZ6L2 expression was inversely correlated with the expression of cytochrome C in malignant tissues in patients with CRC. Collectively, the present study indicates that SEZ6L2 is a potential prognosis biomarker and therapy target for CRC.

Indexed as

AnimalsApoptosisBiomarkers, TumorCaspasesCell Line, TumorCell MovementCell ProliferationColorectal NeoplasmsFemaleFlow CytometryGene Expression Regulation, NeoplasticGene Knockdown TechniquesHeterograftsHumansMaleMembrane ProteinsBiomarkers, TumorCaspasesMembrane ProteinsSEZ6L2 protein, humanapoptosiscaspasecolorectal cancermitochondriaprognosisSEZ6L2

Identifiers

PMID32105413
PMCPMC7171412
OpenAlexW3007433668

What OpenQuestion holds

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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.