Evidence map›Paper›PMID 29530061›Full record

ArticleJournal of experimental & clinical cancer research : CR2018

Stearoyl-CoA desaturase-1 promotes colorectal cancer metastasis in response to glucose by suppressing PTEN.

Hui Ran, Yemin Zhu, Ruyuan Deng, Qi Zhang, Xisheng Liu, Ming Feng, Jie Zhong, Shuhai Lin, Xuemei Tong, Qing Su

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 82 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

82 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.

  1. Pooled it
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  9. Cancer metastasisFrontiers in bioengineering and biotechnology · 2026
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22 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Hui RanDepartment of Endocrinology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, 1665, Kong Jiang Road, Shanghai, 200092, China.
Yemin ZhuDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, 280 S. Chongqing Road, Shanghai, 200025, China.
Ruyuan DengDepartment of Endocrinology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, 1665, Kong Jiang Road, Shanghai, 200092, China.
Qi ZhangDepartment of Endocrinology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, 1665, Kong Jiang Road, Shanghai, 200092, China.
Xisheng LiuDepartment of General Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, 100, Haining Road, Shanghai, 200080, China.
Ming FengDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, 280 S. Chongqing Road, Shanghai, 200025, China.
Jie ZhongDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, 280 S. Chongqing Road, Shanghai, 200025, China.
Shuhai LinDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, 280 S. Chongqing Road, Shanghai, 200025, China.
Xuemei TongDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, 280 S. Chongqing Road, Shanghai, 200025, China. xuemeitong@shsmu.edu.cn.
Qing SuDepartment of Endocrinology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, 1665, Kong Jiang Road, Shanghai, 200092, China. suqing@xinhuamed.com.cn.
Shanghai Jiao Tong University · CNXinHua Hospital · CNShanghai First People's Hospital · CN

Funding

Clinical Research Plan of SHDC 16CR4012ANational Key Research Program of China No. 2016YFC1304800National Natural Science Foundation of China 81370935National Natural Science Foundation of China 81472239National Natural Science Foundation of China 81670743National Natural Science Foundation of China 81672322Shanghai Education Committee Key Program 14zz110Shanghai Municipal Commission of Health and Family Planning for Youth 20154Y0084Shanghai Municipal Health Bureau Planning for Youth 20134Y136
6 · The paper itself

Abstract

backgroundDiabetic patients have a higher risk factor for colorectal cancer (CRC) metastasis. Stearoyl-CoA desaturase 1 (SCD1), the main enzyme responsible for producing monounsaturated fatty acids(MUFA) from saturated fatty acids, is frequently deregulated in both diabetes and CRC. The function and mechanism of SCD1 in metastasis of CRC and its relevance to glucose remains largely unknown.

methodsSCD1 expression levels were analyzed in human CRC tissues and the Cancer Browser database ( https://genome-cancer.ucsc.edu/ ). CRC cell lines stably transfected with SCD1 shRNAs or vector were established to investigate the role of SCD1 in modulating migration and invasion of CRC cells. A glucose concentration gradient was set to investigate regulation of SCD1 in CRC relevant to diabetic conditions.

resultsThe clinical data analysis showed high expression of SCD1 in CRC tissues with a negative correlation with the prognosis of CRC. In vitro experiments revealed that SCD1 increased CRC progression through promoting epithelial-mesenchymal transition (EMT). Lipidomic analysis demonstrated that SCD1 increased MUFA levels and MUFA administration could rescue migration and invasion defect of CRC cells induced by SCD1 knockdown. Furthermore, SCD1-mediated progression of CRC was promoted by carbohydrate response-element binding protein (ChREBP) in response to high glucose. Mechanistically, hyperglycemia-SCD1-MUFA induced CRC cell migration and invasion by regulating PTEN.

conclusionsOur findings show that SCD1 promotes metastasis of CRC cells through MUFA production and suppressing PTEN in response to glucose, which may be a novel mechanism for diabetes-induced CRC metastasis.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedAnimalsBiomarkers, TumorCell LineCell MovementColorectal NeoplasmsDisease Models, AnimalEpithelial-Mesenchymal TransitionFatty Acids, MonounsaturatedFemaleGlucoseHumansMaleMiceBiomarkers, TumorFatty Acids, MonounsaturatedGlucosePTEN PhosphohydrolasePTEN protein, humanSCD1 protein, humanStearoyl-CoA DesaturaseChREBPColorectal cancerHigh glucoseMetastasisPTENSCD1

Identifiers

PMID29530061
PMCPMC5848567
OpenAlexW2801015037

What Socratic 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 Socratic graph.