ChloroquineV1, PubMed, Corpus, bibRecord, 000203

Tumour-initiating cell-specific miR-1246 and miR-1290 expression converge to promote non-small cell lung cancer progression.

Identifieur interne : 000203 ( PubMed/Corpus ); précédent : 000202; suivant : 000204

Tumour-initiating cell-specific miR-1246 and miR-1290 expression converge to promote non-small cell lung cancer progression.

Auteurs : Wen Cai Zhang ; Tan Min Chin ; Henry Yang ; Min En Nga ; Declan Patrick Lunny ; Edwin Kok Hao Lim ; Li Li Sun ; Yin Huei Pang ; Yi Ning Leow ; Shanneen Rossellini Y. Malusay ; Priscilla Xin Hui Lim ; Jeravan Zili Lee ; Benedict Jian Wei Tan ; Ng Shyh-Chang ; Elaine Hsuen Lim ; Wan Teck Lim ; Daniel Shao Weng Tan ; Eng Huat Tan ; Bee Choo Tai ; Ross Andrew Soo ; Wai Leong Tam ; Bing Lim

Source :

Nature communications [ 2041-1723 ] ; 2016.

RBID : pubmed:27325363

English descriptors

KwdEn :
- A549 Cells, Animals, Antineoplastic Combined Chemotherapy Protocols (pharmacology), Carcinoma, Non-Small-Cell Lung (genetics), Carcinoma, Non-Small-Cell Lung (metabolism), Carcinoma, Non-Small-Cell Lung (pathology), Carcinoma, Non-Small-Cell Lung (therapy), Disease Progression, Female, Gefitinib, Gene Expression Regulation, Neoplastic, HEK293 Cells, Humans, Hydroxychloroquine (pharmacology), Lung Neoplasms (genetics), Lung Neoplasms (metabolism), Lung Neoplasms (pathology), Lung Neoplasms (therapy), Lymphatic Metastasis, Mice, MicroRNAs (antagonists & inhibitors), MicroRNAs (genetics), MicroRNAs (metabolism), Neoplastic Stem Cells (metabolism), Neoplastic Stem Cells (pathology), Oligonucleotides (administration & dosage), Oligonucleotides (genetics), Oligonucleotides (metabolism), Quinazolines (pharmacology), Signal Transduction, Survival Analysis, Tumor Burden, Xenograft Model Antitumor Assays.
MESH :
- chemical , administration & dosage : Oligonucleotides.
- chemical , antagonists & inhibitors : MicroRNAs.
- chemical , genetics : MicroRNAs, Oligonucleotides.
- chemical , metabolism : MicroRNAs, Oligonucleotides.
- chemical , pharmacology : Hydroxychloroquine, Quinazolines.
- chemical : Gefitinib.
- genetics : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- metabolism : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms, Neoplastic Stem Cells.
- pathology : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms, Neoplastic Stem Cells.
- pharmacology : Antineoplastic Combined Chemotherapy Protocols.
- therapy : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- A549 Cells, Animals, Disease Progression, Female, Gene Expression Regulation, Neoplastic, HEK293 Cells, Humans, Lymphatic Metastasis, Mice, Signal Transduction, Survival Analysis, Tumor Burden, Xenograft Model Antitumor Assays.

Abstract

The tumour-initiating cell (TIC) model accounts for phenotypic and functional heterogeneity among tumour cells. MicroRNAs (miRNAs) are regulatory molecules frequently aberrantly expressed in cancers, and may contribute towards tumour heterogeneity and TIC behaviour. More recent efforts have focused on miRNAs as diagnostic or therapeutic targets. Here, we identified the TIC-specific miRNAs, miR-1246 and miR-1290, as crucial drivers for tumour initiation and cancer progression in human non-small cell lung cancer. The loss of either miRNA impacted the tumour-initiating potential of TICs and their ability to metastasize. Longitudinal analyses of serum miR-1246 and miR-1290 levels across time correlate their circulating levels to the clinical response of lung cancer patients who were receiving ongoing anti-neoplastic therapies. Functionally, direct inhibition of either miRNA with locked nucleic acid administered systemically, can arrest the growth of established patient-derived xenograft tumours, thus indicating that these miRNAs are clinically useful as biomarkers for tracking disease progression and as therapeutic targets.

DOI: 10.1038/ncomms11702
PubMed: 27325363

Links to Exploration step

pubmed:27325363

Le document en format XML

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<term>Carcinoma, Non-Small-Cell Lung (metabolism)</term>
<term>Carcinoma, Non-Small-Cell Lung (pathology)</term>
<term>Carcinoma, Non-Small-Cell Lung (therapy)</term>
<term>Disease Progression</term>
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<term>Gefitinib</term>
<term>Gene Expression Regulation, Neoplastic</term>
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<term>Humans</term>
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<term>Oligonucleotides (administration & dosage)</term>
<term>Oligonucleotides (genetics)</term>
<term>Oligonucleotides (metabolism)</term>
<term>Quinazolines (pharmacology)</term>
<term>Signal Transduction</term>
<term>Survival Analysis</term>
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<front><div type="abstract" xml:lang="en">The tumour-initiating cell (TIC) model accounts for phenotypic and functional heterogeneity among tumour cells. MicroRNAs (miRNAs) are regulatory molecules frequently aberrantly expressed in cancers, and may contribute towards tumour heterogeneity and TIC behaviour. More recent efforts have focused on miRNAs as diagnostic or therapeutic targets. Here, we identified the TIC-specific miRNAs, miR-1246 and miR-1290, as crucial drivers for tumour initiation and cancer progression in human non-small cell lung cancer. The loss of either miRNA impacted the tumour-initiating potential of TICs and their ability to metastasize. Longitudinal analyses of serum miR-1246 and miR-1290 levels across time correlate their circulating levels to the clinical response of lung cancer patients who were receiving ongoing anti-neoplastic therapies. Functionally, direct inhibition of either miRNA with locked nucleic acid administered systemically, can arrest the growth of established patient-derived xenograft tumours, thus indicating that these miRNAs are clinically useful as biomarkers for tracking disease progression and as therapeutic targets.</div>
</front>
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<DateCompleted><Year>2018</Year>
<Month>08</Month>
<Day>21</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>12</Month>
<Day>02</Day>
</DateRevised>
<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2041-1723</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>7</Volume>
<PubDate><Year>2016</Year>
<Month>06</Month>
<Day>21</Day>
</PubDate>
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<Title>Nature communications</Title>
<ISOAbbreviation>Nat Commun</ISOAbbreviation>
</Journal>
<ArticleTitle>Tumour-initiating cell-specific miR-1246 and miR-1290 expression converge to promote non-small cell lung cancer progression.</ArticleTitle>
<Pagination><MedlinePgn>11702</MedlinePgn>
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<Abstract><AbstractText>The tumour-initiating cell (TIC) model accounts for phenotypic and functional heterogeneity among tumour cells. MicroRNAs (miRNAs) are regulatory molecules frequently aberrantly expressed in cancers, and may contribute towards tumour heterogeneity and TIC behaviour. More recent efforts have focused on miRNAs as diagnostic or therapeutic targets. Here, we identified the TIC-specific miRNAs, miR-1246 and miR-1290, as crucial drivers for tumour initiation and cancer progression in human non-small cell lung cancer. The loss of either miRNA impacted the tumour-initiating potential of TICs and their ability to metastasize. Longitudinal analyses of serum miR-1246 and miR-1290 levels across time correlate their circulating levels to the clinical response of lung cancer patients who were receiving ongoing anti-neoplastic therapies. Functionally, direct inhibition of either miRNA with locked nucleic acid administered systemically, can arrest the growth of established patient-derived xenograft tumours, thus indicating that these miRNAs are clinically useful as biomarkers for tracking disease progression and as therapeutic targets.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Wen Cai</ForeName>
<Initials>WC</Initials>
<AffiliationInfo><Affiliation>Genome Institute of Singapore, Singapore 138672, Singapore.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chin</LastName>
<ForeName>Tan Min</ForeName>
<Initials>TM</Initials>
<AffiliationInfo><Affiliation>Cancer Science Institute of Singapore, National University of Singapore, Singapore 117599, Singapore.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Haematology-Oncology, National University Cancer Institute, Singapore 119074, Singapore.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yang</LastName>
<ForeName>Henry</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Cancer Science Institute of Singapore, National University of Singapore, Singapore 117599, Singapore.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Nga</LastName>
<ForeName>Min En</ForeName>
<Initials>ME</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, National University Hospital, Singapore 119074, Singapore.</Affiliation>
</AffiliationInfo>
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<ForeName>Declan Patrick</ForeName>
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<ForeName>Edwin Kok Hao</ForeName>
<Initials>EK</Initials>
<AffiliationInfo><Affiliation>Genome Institute of Singapore, Singapore 138672, Singapore.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Sun</LastName>
<ForeName>Li Li</ForeName>
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<AffiliationInfo><Affiliation>Genome Institute of Singapore, Singapore 138672, Singapore.</Affiliation>
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Tumour-initiating cell-specific miR-1246 and miR-1290 expression converge to promote non-small cell lung cancer progression.

Tumour-initiating cell-specific miR-1246 and miR-1290 expression converge to promote non-small cell lung cancer progression.

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