Evidence map›Paper›PMID 31019378›Full record

ArticleCancer cell international2019

SCD1 is required for EGFR-targeting cancer therapy of lung cancer via re-activation of EGFR/PI3K/AKT signals.

Kelin She, Shenghua Fang, Wei Du, Xingxing Fan, Jiaxi He, Hui Pan, Liyan Huang, Ping He, Jun Huang

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

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  8. Lipids: Driving Forces in the Underlying Biology of Carcinogenesis.ACS pharmacology & translational science · 2025
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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

9 authors at 4 institutions in 2 countries.

Kelin She *1Department of Thoracic Surgery, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Research Institute of Respiratory Disease, China Key Laboratory of Respiratory Disease, National Center for Clinical Trials on Respiratory Diseases, No. 151 Yanjiangxi Road, Guangzhou, Guangdong 510120 China.
Shenghua Fang *3Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou, China.
Wei Du *4Department of Thoracic Surgery, Dongguan People's Hospital, Dongguan, Guangdong China.
Xingxing FanState Key Laboratory of Quality Research in Chinese Medicine, Macau Institute for Applied Research in Medicine and Health, Macau University of Science and Technology, Macau, SAR China.
Jiaxi He1Department of Thoracic Surgery, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Research Institute of Respiratory Disease, China Key Laboratory of Respiratory Disease, National Center for Clinical Trials on Respiratory Diseases, No. 151 Yanjiangxi Road, Guangzhou, Guangdong 510120 China.
Hui Pan1Department of Thoracic Surgery, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Research Institute of Respiratory Disease, China Key Laboratory of Respiratory Disease, National Center for Clinical Trials on Respiratory Diseases, No. 151 Yanjiangxi Road, Guangzhou, Guangdong 510120 China.
Liyan Huang1Department of Thoracic Surgery, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Research Institute of Respiratory Disease, China Key Laboratory of Respiratory Disease, National Center for Clinical Trials on Respiratory Diseases, No. 151 Yanjiangxi Road, Guangzhou, Guangdong 510120 China.
Ping He6Department of Pathology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Jun Huang1Department of Thoracic Surgery, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Research Institute of Respiratory Disease, China Key Laboratory of Respiratory Disease, National Center for Clinical Trials on Respiratory Diseases, No. 151 Yanjiangxi Road, Guangzhou, Guangdong 510120 China.
Guangzhou Medical University · CNFirst Affiliated Hospital of Guangzhou Medical University · CNDongguan People’s Hospital · CNMacau University of Science and Technology · MO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCancer cells are characterized by aberrant activation of lipid biosynthesis, producing saturated fatty acids and monounsaturated fatty acids via stearoyl-CoA desaturases (SCD) for regulating metabolic and signaling platforms. SCD1 overexpression functions as an oncogene in lung cancer and predicts a poor clinical outcome. This study aimed to investigate the role of SCD1 inhibition by EGFR inhibitor (Gefitinib)-based anti-tumor therapy of lung cancer both in vitro and in vivo.

methodsCCK-8 assay was performed to determine cell viability. The SCD1 mRNA level was detected by qPCR. The protein levels were assessed by Western blotting. E-cadherin and N-cadherin levels were determined by immunofluorescence. Apoptosis detection was conducted by flow cytometry. Cell migration or invasion was evaluated by transwell assay. The tumor sizes and tumor volumes were calculated in nude mice by subcutaneous injection of A549 cells transfected with vector of pcDNA3.1-SCD1 or negative control. Expression of Ki-67 was detected by immunohistochemistry.

resultSCD1 up-regulated expression was observed in lung cancer cell lines. Cells with overexpressed SCD1 had high IC50 values for Gefitinib in A549 and H1573 cell lines. Overexpression of SCD1 inhibited Gefitinib-induced apoptosis, decreased cell vitality and impaired ability of migration and invasion, while these effects were counteracted by A939572. Mechanistically, SCD1 promoted the activation of proliferation and metastasis-related EGFR/PI3K/AKT signaling, and up-regulated epithelial to mesenchymal transition (EMT) phenotype in the two cell lines, which was restored by SCD1 inhibition. Furthermore, in spite of EGFR inhibition, overexpression of SCD1 in vivo significantly promoted tumor growth by activating EGFR/PI3K/AKT signaling in tumor tissues, but A939572 treatment restricted SCD1-induced tumor progression and inhibited EMT phenotype of cancer cells in vivo.

conclusionThese findings indicated that inhibition of oncogene SCD1 is required for targeting EGFR therapy in lung cancer.

Indexed as

AKTEGFREMTLung cancerSCD1

Identifiers

PMID31019378
PMCPMC6472070
OpenAlexW2944390367

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.