Evidence map›Paper›PMID 28076844›Full record

ArticleOncotarget2017

Sulforaphane inhibits cancer stem-like cell properties and cisplatin resistance through miR-214-mediated downregulation of c-MYC in non-small cell lung cancer.

Qian-Qian Li, You-Ke Xie, Yue Wu, Lin-Lin Li, Ying Liu, Xiao-Bo Miao, Qiu-Zhen Liu, Kai-Tai Yao, Guang-Hui Xiao

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
4.6field-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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

  1. Pooled it
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  10. A complex microRNA regulatory network may control the HCP5/UTP3/c-Myc/VAMP3 signaling axis.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
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  17. Therapeutic Targeting of MicroRNAs in the Tumor Microenvironment.International journal of molecular sciences · 2021
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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 1 institution in 1 country.

Qian-Qian LiCancer Institute, Southern Medical University, Guangzhou 510515, China.
You-Ke XieCancer Institute, Southern Medical University, Guangzhou 510515, China.
Yue WuCancer Institute, Southern Medical University, Guangzhou 510515, China.
Lin-Lin LiCancer Institute, Southern Medical University, Guangzhou 510515, China.
Ying LiuCancer Institute, Southern Medical University, Guangzhou 510515, China.
Xiao-Bo MiaoCancer Institute, Southern Medical University, Guangzhou 510515, China.
Qiu-Zhen LiuCancer Institute, Southern Medical University, Guangzhou 510515, China.
Kai-Tai YaoCancer Institute, Southern Medical University, Guangzhou 510515, China.
Guang-Hui XiaoCancer Institute, Southern Medical University, Guangzhou 510515, China.
Southern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We herein report that sulforaphane (SFN), a potent anti-cancer and well-tolerated dietary compound, inhibits cancer stem-like cell (CSC) properties and enhances therapeutic efficacy of cisplatin in human non-small cell lung cancer (NSCLC). SFN exerted these functions through upregulation of miR-214, which in turn targets the coding region of c-MYC. This finding was further corroborated by our observations that plasmid or lentiviral vector-mediated expression of 3'UTR-less c-MYC cDNA and cisplatin- or doxorubicin-induced endogenous c-MYC accumulation was similarly suppressed by either SFN or miR-214. Further, we showed that the reported inhibitory effects of SFN on β-catenin are also mediated by miR-214. SFN/miR-214 signaling inhibited CSC properties and enhanced the cytotoxicity of chemotherapeutic drugs in vitro. Experiments with nude mice carrying xenograft tumors showed that SFN sensitized NSCLC cells to cisplatin's efficacy, which is accompanied by inhibition of cisplatin-induced c-MYC accumulation in tumor tissues. Our results provided strong evidence and mechanisms to support consideration of SFN or synthetic derivatives as a therapeutic agent in combination with cisplatin for the treatment of patients with NSCLC and, potentially, other types of c-MYC-addicted tumors.

Indexed as

3' Untranslated RegionsA549 CellsAnimalsAntineoplastic Agentsbeta CateninBlotting, WesternCarcinoma, Non-Small-Cell LungCell LineCell Line, TumorCell SurvivalCisplatinDown-RegulationDoxorubicinDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumans3' Untranslated RegionsAntineoplastic Agentsbeta CateninCisplatinDoxorubicinIsothiocyanatesMicroRNAsMIRN214 microRNA, humanMYC protein, humanProto-Oncogene Proteins c-mycsulforaphaneSulfoxidescisplatinc-MYClung cancermiR-214sulforaphane

Identifiers

PMID28076844
PMCPMC5355326
OpenAlexW2568391148

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.