miR-210-5p promotes epithelial–mesenchymal transition by inhibiting PIK3R5 thereby activating oncogenic autophagy in osteosarcoma cells
Identifieur interne : 000008 ( an2020/Analysis ); précédent : 000007; suivant : 000009miR-210-5p promotes epithelial–mesenchymal transition by inhibiting PIK3R5 thereby activating oncogenic autophagy in osteosarcoma cells
Auteurs : Wei Liu ; Dongdong Jiang ; Fangyi Gong ; Yumin Huang ; Yongjun Luo ; Yuluo Rong ; Jiaxing Wang ; Xuhui Ge ; Chengyue Ji ; Jin Fan ; Weihua CaiSource :
- Cell Death & Disease [ 2041-4889 ] ; 2020.
Abstract
Osteosarcoma (OS) is a malignant bone tumor which occurs mainly in adolescents with frequent pulmonary metastasis and a high mortality rate. Accumulating evidence has indicated that microRNAs (miRNAs) play a vital role in various tumors by modulating target genes as well as signal pathways, and aberrant expression of miRNAs may contribute to OS progression. This study aimed to determine the association between miR-210-5p expression and OS progression and to investigate its potential underlying mechanism. Using reverse transcription-polymerase chain reaction (RT-PCR), miR-210-5p was found to be upregulated in clinical OS specimens and cell lines. Further functional analysis demonstrated that miR-210-5p promoted epithelial–mesenchymal transition (EMT) and induced oncogenic autophagy. Luciferase reporter assay, RNA-ChIP, and western blot analysis confirmed that PIK3R5, an essential regulator in the AKT/mTOR signaling pathway, is a target downstream gene of miR-210-5p. Overexpression or knockdown of PIK3R5 reversed the functional role of overexpression or knockdown of miR-210-5p, respectively. Silencing autophagy-related gene 5 (ATG5) abolished the functional effects of miR-210-5p upregulation or PIK3R5 knockdown in OS cells. In vivo, miR-210-5p overexpression promoted OS tumor growth and pulmonary metastasis. Taken together, our results demonstrated that miR-210-5p promoted EMT and oncogenic autophagy by suppressing the expression of PIK3R5 and regulating the AKT/mTOR signaling pathway. Therefore, inhibition of miR-210-5p may represent a promising treatment for OS.
Url:
DOI: 10.1038/s41419-020-2270-1
PubMed: 32024814
PubMed Central: 7002725
Affiliations:
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PMC:7002725Le document en format XML
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uniqKey="Luo Y" first="Yongjun" last="Luo">Yongjun Luo</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Rong, Yuluo" sort="Rong, Yuluo" uniqKey="Rong Y" first="Yuluo" last="Rong">Yuluo Rong</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Wang, Jiaxing" sort="Wang, Jiaxing" uniqKey="Wang J" first="Jiaxing" last="Wang">Jiaxing Wang</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Ge, Xuhui" sort="Ge, Xuhui" uniqKey="Ge X" first="Xuhui" last="Ge">Xuhui Ge</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Ji, Chengyue" sort="Ji, Chengyue" uniqKey="Ji C" first="Chengyue" last="Ji">Chengyue Ji</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Fan, Jin" sort="Fan, Jin" uniqKey="Fan J" first="Jin" last="Fan">Jin Fan</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Cai, Weihua" sort="Cai, Weihua" uniqKey="Cai W" first="Weihua" last="Cai">Weihua Cai</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">32024814</idno><idno type="pmc">7002725</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7002725</idno><idno type="RBID">PMC:7002725</idno><idno type="doi">10.1038/s41419-020-2270-1</idno><date when="2020">2020</date><idno type="wicri:Area/Pmc/Corpus">000080</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000080</idno><idno type="wicri:Area/Pmc/Curation">000080</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000080</idno><idno type="wicri:Area/Pmc/Checkpoint">000003</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000003</idno><idno 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sort="Gong, Fangyi" uniqKey="Gong F" first="Fangyi" last="Gong">Fangyi Gong</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Huang, Yumin" sort="Huang, Yumin" uniqKey="Huang Y" first="Yumin" last="Huang">Yumin Huang</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Luo, Yongjun" sort="Luo, Yongjun" uniqKey="Luo Y" first="Yongjun" last="Luo">Yongjun Luo</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Rong, Yuluo" sort="Rong, Yuluo" uniqKey="Rong Y" first="Yuluo" last="Rong">Yuluo Rong</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Wang, Jiaxing" sort="Wang, Jiaxing" uniqKey="Wang J" first="Jiaxing" last="Wang">Jiaxing Wang</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Ge, Xuhui" sort="Ge, Xuhui" uniqKey="Ge X" first="Xuhui" last="Ge">Xuhui Ge</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Ji, Chengyue" sort="Ji, Chengyue" uniqKey="Ji C" first="Chengyue" last="Ji">Chengyue Ji</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Fan, Jin" sort="Fan, Jin" uniqKey="Fan J" first="Jin" last="Fan">Jin Fan</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Cai, Weihua" sort="Cai, Weihua" uniqKey="Cai W" first="Weihua" last="Cai">Weihua Cai</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author></analytic><series><title level="j">Cell Death & Disease</title><idno type="eISSN">2041-4889</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="Par1">Osteosarcoma (OS) is a malignant bone tumor which occurs mainly in adolescents with frequent pulmonary metastasis and a high mortality rate. Accumulating evidence has indicated that microRNAs (miRNAs) play a vital role in various tumors by modulating target genes as well as signal pathways, and aberrant expression of miRNAs may contribute to OS progression. This study aimed to determine the association between miR-210-5p expression and OS progression and to investigate its potential underlying mechanism. Using reverse transcription-polymerase chain reaction (RT-PCR), miR-210-5p was found to be upregulated in clinical OS specimens and cell lines. Further functional analysis demonstrated that miR-210-5p promoted epithelial–mesenchymal transition (EMT) and induced oncogenic autophagy. Luciferase reporter assay, RNA-ChIP, and western blot analysis confirmed that PIK3R5, an essential regulator in the AKT/mTOR signaling pathway, is a target downstream gene of miR-210-5p. Overexpression or knockdown of PIK3R5 reversed the functional role of overexpression or knockdown of miR-210-5p, respectively. Silencing autophagy-related gene 5 (ATG5) abolished the functional effects of miR-210-5p upregulation or PIK3R5 knockdown in OS cells. In vivo, miR-210-5p overexpression promoted OS tumor growth and pulmonary metastasis. Taken together, our results demonstrated that miR-210-5p promoted EMT and oncogenic autophagy by suppressing the expression of PIK3R5 and regulating the AKT/mTOR signaling pathway. Therefore, inhibition of miR-210-5p may represent a promising treatment for OS.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Ritter, J" uniqKey="Ritter J">J Ritter</name></author><author><name sortKey="Bielack, Ss" uniqKey="Bielack S">SS Bielack</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ottaviani, G" uniqKey="Ottaviani G">G Ottaviani</name></author><author><name sortKey="Jaffe, N" uniqKey="Jaffe N">N Jaffe</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Aljubran, Ah" uniqKey="Aljubran A">AH Aljubran</name></author><author><name sortKey="Griffin, A" uniqKey="Griffin A">A Griffin</name></author><author><name sortKey="Pintilie, M" uniqKey="Pintilie M">M Pintilie</name></author><author><name sortKey="Blackstein, M" uniqKey="Blackstein M">M Blackstein</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Luetke, A" 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|flux= an2020
|étape= Analysis
|type= RBID
|clé= PMC:7002725
|texte= miR-210-5p promotes epithelial–mesenchymal transition by inhibiting PIK3R5 thereby activating oncogenic autophagy in osteosarcoma cells
}}
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