Open AccessLnc RNA PLAC 2 down‐regulates RPL 36 expression and blocks cell cycle progression in glioma through a mechanism involving STAT 1
Author(s) -
Hu YanWei,
Kang ChunMin,
Zhao JingJing,
Nie Ying,
Zheng Lei,
Li HaiXia,
Li Xin,
Wang Qian,
Qiu YuRong
Publication year - 2018
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13338
Subject(s) - glioma , cell cycle , cell growth , rna , cell cycle checkpoint , long non coding rna , biology , stat protein , cancer research , carcinogenesis , microbiology and biotechnology , stat , cell , transcription (linguistics) , chemistry , signal transduction , stat3 , cancer , biochemistry , genetics , gene , linguistics , philosophy
Current glioma therapies allow in situ delivery of cytotoxic drugs to the tumour; however, gliomas show early recurrence due to their highly proliferative character. Long non‐coding (lnc) RNA s play critical roles in tumorigenesis by controlling cell proliferation and cycling. However, the mechanism of action of lnc RNA s in glioma development remains unclear. Here, we report that the lnc RNA PLAC 2 induces cell cycle arrest by targeting ribosomal protein ( RP )L36 in glioma. RPL 36 promoted cell proliferation and G1/S cell cycle progression. Mass spectrometry analysis revealed that signal transducer and activator of transcription ( STAT )1 interacted with both lnc RNA PLAC 2 and the RPL 36 promoter. We also found that the nucleus PLAC 2 bind with STAT 1 and interact with RPL 36 promoters but the cytoplasmic lnc RNA PLAC 2 inhibited STAT 1 nuclear transfer, thereby decreasing RP 36 expression, inhibiting cell proliferation and inducing cell cycle arrest. These results provide evidence for a novel cell cycle regulatory network in glioma comprising the lnc RNA PLAC 2 along with STAT 1 and RPL 36 that can serve as a therapeutic target for glioma treatment.