Abstract:
:A great deal of evidence suggests that long non-coding RNAs (lncRNAs) function in the tumorigenesis of retinoblastoma (RB). However, the roles of lncRNA ILF3-AS1 in RB are still unclear. In the present study, our work revealed that the lncRNA ILF3-AS1 was increased in both RB tissues and cell lines. Repression of ILF3-AS1 suppressed both RB cell proliferation and invasion in vitro. ILF3-AS1 also promoted tumor growth in vivo. While exploring the mechanisms behind ILF3-AS1 in RB, we identified that ILF3-AS1 sponges with miR-132-3p that is expressed at low levels in RB tissues as well as attenuates RB progression. Furthermore, SMAD2 was confirmed to be a miR-132-3p target. Finally, we found that SMAD2 overexpression or miR-132-3p inhibitors recover the inhibitory effects of ILF3-AS1 suppression on RB progression. Collectively, these data indicate that ILF3-AS1 is involved in RB progression through the miR-132-3p/SMAD2 axis, providing a novel and promising biomarker that can be used for the treatment of RB.
journal_name
Exp Cell Resjournal_title
Experimental cell researchauthors
Han S,Song L,Chen Y,Hou M,Wei X,Fan Ddoi
10.1016/j.yexcr.2020.112087subject
Has Abstractpub_date
2020-08-15 00:00:00pages
112087issue
2eissn
0014-4827issn
1090-2422pii
S0014-4827(20)30329-3journal_volume
393pub_type
杂志文章abstract::We have studied the use of electrofusion to obtain hybridomas producing antigen-specific antibodies after immunization of murine lymphocytes in vitro. Under optimal conditions fusion frequencies of the order of magnitude of 10(-3) were obtained, which is approximately 80-fold higher than the mean value obtained with f...
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