The long noncoding RNA H19 promotes tamoxifen resistance in breast cancer via autophagy
Identifieur interne : 000341 ( Main/Exploration ); précédent : 000340; suivant : 000342The long noncoding RNA H19 promotes tamoxifen resistance in breast cancer via autophagy
Auteurs : Ji Wang ; Shuduo Xie ; Jingjing Yang ; Hanchu Xiong ; Yunlu Jia ; Yulu Zhou ; Yongxia Chen ; Xiaogang Ying ; Cong Chen ; Chenyang Ye [République populaire de Chine] ; Linbo Wang ; Jichun ZhouSource :
- Journal of Hematology & Oncology [ 1756-8722 ] ; 2019.
Abstract
Tamoxifen resistance remains a clinical challenge for hormone receptor-positive breast cancer. Recently, dysregulations in autophagy have been suggested as a potential mechanism for tamoxifen resistance. Although the long noncoding RNA H19 is involved in various stages of tumorigenesis, its role in tamoxifen resistance remains unknown. Here, we assessed the role of H19 in the development of tamoxifen-resistant breast cancer.
Quantitative real-time PCR analyzed expression of H19 in tamoxifen-resistant breast cancer tissues. Knockdown of H19 was used to assess the sensitivity to tamoxifen in vitro and in vivo. Both knockdown and overexpression of H19 were used to analyze the status of autophagy. Real-time quantitative methylation-specific polymerase chain reaction, chromatin immunoprecipitation, immunofluorescence, and Western blot were used to explore the tamoxifen resistance mechanism of H19.
In this study, we observed that the expression of H19 was substantially upregulated in tamoxifen-resistant breast cancer cell line and tumor tissues, and knockdown of H19 enhanced the sensitivity to tamoxifen both in vitro and in vivo. Furthermore, knockdown of H19 significantly inhibited autophagy in MCF7 tamoxifen-resistant (MCF7/TAMR) cells. Conversely, overexpression of H19 promoted autophagy. Interestingly, overexpression of H19 in MCF7 tamoxifen-sensitive cells could recapitulate tamoxifen resistance. Moreover, an increase in methylation in the promoter region of Beclin1 was observed in MCF7/TAMR-shH19 cells. In the double knockdown groups, both shH19+shSAHH and shH19+shDNMT3B rescued the Beclin1 promoter region methylation levels and reactivated autophagy functions. A chromatin immunoprecipitation assay further validated that DNMT3B binds to the Beclin1 promoter region and the knockdown of H19 increases this binding.
Our findings demonstrate that H19 induces autophagy activation
The online version of this article (10.1186/s13045-019-0747-0) contains supplementary material, which is available to authorized users.
Url:
DOI: 10.1186/s13045-019-0747-0
PubMed: 31340867
PubMed Central: 6657081
Affiliations:
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Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">The long noncoding RNA H19 promotes tamoxifen resistance in breast cancer <italic>via</italic>
autophagy</title>
<author><name sortKey="Wang, Ji" sort="Wang, Ji" uniqKey="Wang J" first="Ji" last="Wang">Ji Wang</name>
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<author><name sortKey="Xie, Shuduo" sort="Xie, Shuduo" uniqKey="Xie S" first="Shuduo" last="Xie">Shuduo Xie</name>
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</affiliation>
</author>
<author><name sortKey="Wang, Linbo" sort="Wang, Linbo" uniqKey="Wang L" first="Linbo" last="Wang">Linbo Wang</name>
<affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1759 700X</institution-id>
<institution-id institution-id-type="GRID">grid.13402.34</institution-id>
<institution>Department of Surgical Oncology, Sir Run Run Shaw Hospital,</institution>
<institution>Zhejiang University School of Medicine,</institution>
</institution-wrap>
No.3 Eastern Qingchun Road, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="Aff2">Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Zhou, Jichun" sort="Zhou, Jichun" uniqKey="Zhou J" first="Jichun" last="Zhou">Jichun Zhou</name>
<affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1759 700X</institution-id>
<institution-id institution-id-type="GRID">grid.13402.34</institution-id>
<institution>Department of Surgical Oncology, Sir Run Run Shaw Hospital,</institution>
<institution>Zhejiang University School of Medicine,</institution>
</institution-wrap>
No.3 Eastern Qingchun Road, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="Aff2">Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
</author>
</analytic>
<series><title level="j">Journal of Hematology & Oncology</title>
<idno type="eISSN">1756-8722</idno>
<imprint><date when="2019">2019</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p id="Par1">Tamoxifen resistance remains a clinical challenge for hormone receptor-positive breast cancer. Recently, dysregulations in autophagy have been suggested as a potential mechanism for tamoxifen resistance. Although the long noncoding RNA H19 is involved in various stages of tumorigenesis, its role in tamoxifen resistance remains unknown. Here, we assessed the role of H19 in the development of tamoxifen-resistant breast cancer.</p>
</sec>
<sec><title>Methods</title>
<p id="Par2">Quantitative real-time PCR analyzed expression of H19 in tamoxifen-resistant breast cancer tissues. Knockdown of H19 was used to assess the sensitivity to tamoxifen in vitro and in vivo. Both knockdown and overexpression of H19 were used to analyze the status of autophagy. Real-time quantitative methylation-specific polymerase chain reaction, chromatin immunoprecipitation, immunofluorescence, and Western blot were used to explore the tamoxifen resistance mechanism of H19.</p>
</sec>
<sec><title>Results</title>
<p id="Par3">In this study, we observed that the expression of H19 was substantially upregulated in tamoxifen-resistant breast cancer cell line and tumor tissues, and knockdown of H19 enhanced the sensitivity to tamoxifen both in vitro and in vivo. Furthermore, knockdown of H19 significantly inhibited autophagy in MCF7 tamoxifen-resistant (MCF7/TAMR) cells. Conversely, overexpression of H19 promoted autophagy. Interestingly, overexpression of H19 in MCF7 tamoxifen-sensitive cells could recapitulate tamoxifen resistance. Moreover, an increase in methylation in the promoter region of Beclin1 was observed in MCF7/TAMR-shH19 cells. In the double knockdown groups, both shH19+shSAHH and shH19+shDNMT3B rescued the Beclin1 promoter region methylation levels and reactivated autophagy functions. A chromatin immunoprecipitation assay further validated that DNMT3B binds to the Beclin1 promoter region and the knockdown of H19 increases this binding.</p>
</sec>
<sec><title>Conclusions</title>
<p id="Par4">Our findings demonstrate that H19 induces autophagy activation <italic>via</italic>
the H19/SAHH/DNMT3B axis, which could contribute to tamoxifen resistance in breast cancer.</p>
</sec>
<sec><title>Electronic supplementary material</title>
<p>The online version of this article (10.1186/s13045-019-0747-0) contains supplementary material, which is available to authorized users.</p>
</sec>
</div>
</front>
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