Exosome-transmitted miR-567 reverses trastuzumab resistance by inhibiting ATG5 in breast cancer
Identifieur interne : 000157 ( an2020/Analysis ); précédent : 000156; suivant : 000158Exosome-transmitted miR-567 reverses trastuzumab resistance by inhibiting ATG5 in breast cancer
Auteurs : Mingli Han [République populaire de Chine] ; Jianguo Hu [République populaire de Chine] ; Pengwei Lu [République populaire de Chine] ; Hui Cao [République populaire de Chine] ; Chao Yu [République populaire de Chine] ; Xiangke Li [République populaire de Chine] ; Xueke Qian [République populaire de Chine] ; Xue Yang [République populaire de Chine] ; Yunqing Yang [République populaire de Chine] ; Na Han [République populaire de Chine] ; Dongwei Dou [République populaire de Chine] ; Fan Zhang [République populaire de Chine] ; Mulin Ye [République populaire de Chine] ; Changcheng Yang [République populaire de Chine] ; Yuanting Gu [République populaire de Chine] ; Huaying Dong [République populaire de Chine]Source :
- Cell Death & Disease [ 2041-4889 ] ; 2020.
Abstract
Trastuzumab is commonly used in the treatment of human epidermal growth factor receptor-2 positive (HER-2+) breast cancer, but its efficacy is often limited by the emergence of chemoresistance. Recent studies indicate that exosomes act as vehicles for exchange of genetic cargo between heterogeneous populations of tumor cells, engendering a transmitted drug resistance for cancer development and progression. However, the specific contribution of breast cancer-derived exosomes is poorly understood. In this study, publicly available expression profiling data from breast cancer and bioinformatics analyses were used to screen potential miRNAs in trastuzumab resistance. A series of gain- or loss-functional assays were performed to define the function of miR-567 and ATG5 in trastuzumab resistance and autophagy, both in vitro and in vivo. Our results showed that miR-567 was significantly decreased in trastuzumab-resistant patients compared with responding patients. Moreover, miR-567 was also downregulated in trastuzumab-resistant cells compared with parental cells. Overexpression of miR-567 reversed chemoresistance, whereas silence of miR-567 induced trastuzumab resistance, both in vitro and in vivo. In addition, enhanced miR-567 could be packaged into exosomes, incorporated into receipt cells, suppressing autophagy and reversed chemoresistance by targeting ATG5. To conclude, exosomal miR-567 plays a key role in reversing trastuzumab resistance via regulating autophagy, indicating it may be a promising therapeutic target and prognostic indicator for breast cancer patients.
Url:
DOI: 10.1038/s41419-020-2250-5
PubMed: 31969559
PubMed Central: 6976584
Affiliations:
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PMC:6976584Le document en format XML
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Zhengzhou, 450052 China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Zhengzhou</wicri:regionArea>
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Haikou, 570311 China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Haikou</wicri:regionArea>
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<author><name sortKey="Ye, Mulin" sort="Ye, Mulin" uniqKey="Ye M" first="Mulin" last="Ye">Mulin Ye</name>
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<institution>Department of General Surgery, Hainan General Hospital,</institution>
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</institution-wrap>
Haikou, 570311 China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Haikou</wicri:regionArea>
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<author><name sortKey="Yang, Changcheng" sort="Yang, Changcheng" uniqKey="Yang C" first="Changcheng" last="Yang">Changcheng Yang</name>
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<institution-id institution-id-type="GRID">grid.443397.e</institution-id>
<institution>Department of Oncology,</institution>
<institution>The First Affiliated Hospital of Hainan Medical University,</institution>
</institution-wrap>
Haikou, 570102 China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Haikou</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Gu, Yuanting" sort="Gu, Yuanting" uniqKey="Gu Y" first="Yuanting" last="Gu">Yuanting Gu</name>
<affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.412633.1</institution-id>
<institution>Department of Breast Surgery,</institution>
<institution>The First Affiliated Hospital of Zhengzhou University,</institution>
</institution-wrap>
Zhengzhou, 450052 China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Zhengzhou</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Dong, Huaying" sort="Dong, Huaying" uniqKey="Dong H" first="Huaying" last="Dong">Huaying Dong</name>
<affiliation wicri:level="1"><nlm:aff id="Aff6"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 0368 7493</institution-id>
<institution-id institution-id-type="GRID">grid.443397.e</institution-id>
<institution>Department of General Surgery, Hainan General Hospital,</institution>
<institution>Hainan Affiliated Hospital of Hainan Medical University,</institution>
</institution-wrap>
Haikou, 570311 China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Haikou</wicri:regionArea>
</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>
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<front><div type="abstract" xml:lang="en"><p id="Par1">Trastuzumab is commonly used in the treatment of human epidermal growth factor receptor-2 positive (HER-2+) breast cancer, but its efficacy is often limited by the emergence of chemoresistance. Recent studies indicate that exosomes act as vehicles for exchange of genetic cargo between heterogeneous populations of tumor cells, engendering a transmitted drug resistance for cancer development and progression. However, the specific contribution of breast cancer-derived exosomes is poorly understood. In this study, publicly available expression profiling data from breast cancer and bioinformatics analyses were used to screen potential miRNAs in trastuzumab resistance. A series of gain- or loss-functional assays were performed to define the function of miR-567 and ATG5 in trastuzumab resistance and autophagy, both in vitro and in vivo. Our results showed that miR-567 was significantly decreased in trastuzumab-resistant patients compared with responding patients. Moreover, miR-567 was also downregulated in trastuzumab-resistant cells compared with parental cells. Overexpression of miR-567 reversed chemoresistance, whereas silence of miR-567 induced trastuzumab resistance, both in vitro and in vivo. In addition, enhanced miR-567 could be packaged into exosomes, incorporated into receipt cells, suppressing autophagy and reversed chemoresistance by targeting ATG5. To conclude, exosomal miR-567 plays a key role in reversing trastuzumab resistance via regulating autophagy, indicating it may be a promising therapeutic target and prognostic indicator for breast cancer patients.</p>
</div>
</front>
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</back>
</TEI>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
</list>
<tree><country name="République populaire de Chine"><noRegion><name sortKey="Han, Mingli" sort="Han, Mingli" uniqKey="Han M" first="Mingli" last="Han">Mingli Han</name>
</noRegion>
<name sortKey="Cao, Hui" sort="Cao, Hui" uniqKey="Cao H" first="Hui" last="Cao">Hui Cao</name>
<name sortKey="Dong, Huaying" sort="Dong, Huaying" uniqKey="Dong H" first="Huaying" last="Dong">Huaying Dong</name>
<name sortKey="Dou, Dongwei" sort="Dou, Dongwei" uniqKey="Dou D" first="Dongwei" last="Dou">Dongwei Dou</name>
<name sortKey="Gu, Yuanting" sort="Gu, Yuanting" uniqKey="Gu Y" first="Yuanting" last="Gu">Yuanting Gu</name>
<name sortKey="Han, Na" sort="Han, Na" uniqKey="Han N" first="Na" last="Han">Na Han</name>
<name sortKey="Hu, Jianguo" sort="Hu, Jianguo" uniqKey="Hu J" first="Jianguo" last="Hu">Jianguo Hu</name>
<name sortKey="Li, Xiangke" sort="Li, Xiangke" uniqKey="Li X" first="Xiangke" last="Li">Xiangke Li</name>
<name sortKey="Lu, Pengwei" sort="Lu, Pengwei" uniqKey="Lu P" first="Pengwei" last="Lu">Pengwei Lu</name>
<name sortKey="Qian, Xueke" sort="Qian, Xueke" uniqKey="Qian X" first="Xueke" last="Qian">Xueke Qian</name>
<name sortKey="Yang, Changcheng" sort="Yang, Changcheng" uniqKey="Yang C" first="Changcheng" last="Yang">Changcheng Yang</name>
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<name sortKey="Yu, Chao" sort="Yu, Chao" uniqKey="Yu C" first="Chao" last="Yu">Chao Yu</name>
<name sortKey="Zhang, Fan" sort="Zhang, Fan" uniqKey="Zhang F" first="Fan" last="Zhang">Fan Zhang</name>
</country>
</tree>
</affiliations>
</record>
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