Evidence map›Paper›PMID 34268906›Full record

ArticleCancer communications (London, England)2021

Squalene epoxidase promotes colorectal cancer cell proliferation through accumulating calcitriol and activating CYP24A1-mediated MAPK signaling.

Luwei He, Huaguang Li, Chenyu Pan, Yutong Hua, Jiayin Peng, Zhaocai Zhou, Yun Zhao, Moubin Lin

Open access · goldAbstract read
In one paragraph

Article in Cancer communications (London, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 4% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Squalene Epoxidase: Its Regulations and Links with Cancers.International journal of molecular sciences · 2024
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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 at 3 institutions in 1 country.

Luwei HeCenter for Clinical Research and Translational Medicine, Yangpu Hospital, Tongji University School of Medicine, Shanghai, 200090, P. R. China.ORCID 0000-0001-6564-848X
Huaguang LiCenter for Clinical Research and Translational Medicine, Yangpu Hospital, Tongji University School of Medicine, Shanghai, 200090, P. R. China.
Chenyu PanCenter for Clinical Research and Translational Medicine, Yangpu Hospital, Tongji University School of Medicine, Shanghai, 200090, P. R. China.
Yutong HuaCenter for Clinical Research and Translational Medicine, Yangpu Hospital, Tongji University School of Medicine, Shanghai, 200090, P. R. China.
Jiayin PengThe State Key Laboratory of Cell Biology, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, P. R. China.
Zhaocai ZhouState Key Laboratory of Genetic Engineering, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai, 200438, P. R. China.
Yun ZhaoThe State Key Laboratory of Cell Biology, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, P. R. China.
Moubin LinCenter for Clinical Research and Translational Medicine, Yangpu Hospital, Tongji University School of Medicine, Shanghai, 200090, P. R. China.
Tongji University · CNChinese Academy of Sciences · CNFudan University · CN

Funding

National Natural Science Foundation of China 31630047National Natural Science Foundation of China 81725014National Natural Science Foundation of China 81874201Natural Science Foundation of Shanghai 20ZR1452300Shanghai Municipal Health Bureau 201840359The National Key Research and Development Program of China 2017YFA0503600The National Key Research and Development Program of China 2020YFA0509000
6 · The paper itself

Abstract

backgroundColorectal cancer (CRC) is one of the most malignant tumors with high incidence, yet its molecular mechanism is not fully understood, hindering the development of targeted therapy. Metabolic abnormalities are a hallmark of cancer. Targeting dysregulated metabolic features has become an important direction for modern anticancer therapy. In this study, we aimed to identify a new metabolic enzyme that promotes proliferation of CRC and to examine the related molecular mechanisms.

methodsWe performed RNA sequencing and tissue microarray analyses of human CRC samples to identify new genes involved in CRC. Squalene epoxidase (SQLE) was identified to be highly upregulated in CRC patients. The regulatory function of SQLE in CRC progression and the therapeutic effect of SQLE inhibitors were determined by measuring CRC cell viability, colony and organoid formation, intracellular cholesterol concentration and xenograft tumor growth. The molecular mechanism of SQLE function was explored by combining transcriptome and untargeted metabolomics analysis. Western blotting and real-time PCR were used to assess MAPK signaling activation by SQLE.

resultsSQLE-related control of cholesterol biosynthesis was highly upregulated in CRC patients and associated with poor prognosis. SQLE promoted CRC growth in vitro and in vivo. Inhibition of SQLE reduced the levels of calcitriol (active form of vitamin D3) and CYP24A1, followed by an increase in intracellular Ca

conclusionsOur findings demonstrate that SQLE promotes CRC through the accumulation of calcitriol and stimulation of CYP24A1-mediated MAPK signaling, highlighting SQLE as a potential therapeutic target for CRC treatment.

Indexed as

Colorectal NeoplasmsSqualene MonooxygenaseCalcitriolCell ProliferationHumansVitamin D3 24-HydroxylaseCalcitriolCYP24A1 protein, humanSqualene MonooxygenaseVitamin D3 24-Hydroxylasecalcitriolcell proliferationcholesterol biosynthesiscolorectal cancerCYP24A1MAPK signalingsqualene epoxidaseterbinafine

Identifiers

PMID34268906
PMCPMC8360641
OpenAlexW3181872499

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.