Exosomal lncRNA H19 promotes the progression of hepatocellular carcinoma treated with Propofol via miR‐520a‐3p/LIMK1 axis
Exosome
DOI:
10.1002/cam4.3313
Publication Date:
2020-08-07T20:47:51Z
AUTHORS (8)
ABSTRACT
Abstract Background Hepatocellular carcinoma (HCC) is one of the leading causes cancer‐related deaths globally. Herein, we explored underlying mechanism by which Propofol inhibited development HCC. Methods 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay was carried out to detect viability and proliferation. Quantitative real‐time polymerase chain reaction (qRT‐PCR) Western blot were performed expression long noncoding RNA (lncRNA) H19, microRNA‐520a‐3p (miR‐520a‐3p), LIM domain kinase 1 (LIMK1), metastasis‐associated markers (Snail, Twist, Vimentin E‐cadherin) exosome (CD9 CD81). Transmission electron microscopy (TEM) used observe morphology structure exosomes. The apoptosis metastasis measured flow cytometry transwell assays. StarBase software utilized predict targets H19 miR‐520a‐3p. Dual‐luciferase reporter confirm interaction between miR‐520a‐3p or LIMK1. Nude mice bearing tumors validate role exosomal H19. RESULTS high accelerated proliferation motility while hampering HCC cells. MiR‐520a‐3p could bind with Exosomal exacerbated through sponging 3’ untranslated region (3’UTR) LIMK1 mimic transfection reversed inhibitory effect on cells promoting effects mRNA protein levels regulated H19/miR‐520a‐3p signaling. level promoted growth in vivo. Conclusion Circulating proliferation, migration invasion treated upregulating via
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