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Exosomal miR-1260b derived from non-small cell lung cancer promotes tumor metastasis through the inhibition of HIPK2

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Abstract
Tumor-derived exosomes (TEXs) contain enriched miRNAs, and exosomal miRNAs can affect tumor growth, including cell proliferation, metastasis, and drug resistance through cell-to-cell communication. We investigated the role of exosomal miR-1260b derived from non-small cell lung cancer (NSCLC) in tumor progression. Exosomal miR-1260b induced angiogenesis by targeting homeodomain-interacting protein kinase-2 (HIPK2) in human umbilical vein endothelial cells (HUVECs). Furthermore, exosomal miR-1260b or suppression of HIPK2 led to enhanced cellular mobility and cisplatin resistance in NSCLC cells. In patients with NSCLC, the level of HIPK2 was significantly lower in tumor tissues than in normal lung tissues, while that of miR-1260b was higher in tumor tissues. HIPK2 and miR-1260b expression showed an inverse correlation, and this correlation was strong in distant metastasis. Finally, the expression level of exosomal miR-1260b in plasma was higher in patients with NSCLC than in healthy individuals, and higher levels of exosomal miR-1260b were associated with high-grade disease, metastasis, and poor survival. In conclusion, exosomal miR-1260b can promote angiogenesis in HUVECs and metastasis of NSCLC by regulating HIPK2 and may serve as a prognostic marker for lung cancers.
Author(s)
김동하박효정최윤정강명희김태근백찬기최창민이재철노진경
Issued Date
2021
Type
Article
Keyword
exosomemiR-1260bnon-small cell lung cancerHIPK2metastasis
DOI
10.1038/s41419-021-04024-9
URI
https://oak.ulsan.ac.kr/handle/2021.oak/9577
https://ulsan-primo.hosted.exlibrisgroup.com/primo-explore/fulldisplay?docid=TN_cdi_doaj_primary_oai_doaj_org_article_dca042ad4e0344bb8fd7320f676e8ec6&context=PC&vid=ULSAN&lang=ko_KR&search_scope=default_scope&adaptor=primo_central_multiple_fe&tab=default_tab&query=any,contains,Exosomal%20miR-1260b%20derived%20from%20non-small%20cell%20lung%20cancer%20promotes%20tumor%20metastasis%20through%20the%20inhibition%20of%20HIPK2&offset=0&pcAvailability=true
Publisher
CELL DEATH DISEASE
Location
독일
Language
영어
ISSN
2041-4889
Citation Volume
12
Citation Number
8
Citation Start Page
0
Citation End Page
0
Appears in Collections:
Natural Science > Biological Sciences
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