Open AccessMicroRNA‐124‐3p regulates cell proliferation, invasion, apoptosis, and bioenergetics by targeting PIM1 in astrocytoma
Author(s) -
Deng Danni,
Wang Lei,
Chen Yao,
Li Bowen,
Xue Lian,
Shao Naiyuan,
Wang Qiang,
Xia Xiwei,
Yang Yilin,
Zhi Feng
Publication year - 2016
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.12946
Subject(s) - microrna , biology , downregulation and upregulation , cell growth , cancer research , untranslated region , three prime untranslated region , cell cycle , messenger rna , apoptosis , microbiology and biotechnology , gene , biochemistry
The PIM 1 protein is an important regulator of cell proliferation, the cell cycle, apoptosis, and metabolism in various human cancers. Micro RNA s (mi RNA s) are powerful post‐transcriptional gene regulators that function through translational repression or transcript destabilization. Therefore, we aimed to identify whether a close relationship exists between PIM 1 and mi RNA s. PIM 1 protein levels and mRNA levels were significantly upregulated in astrocytoma tissues, indicating the oncogenic role of PIM 1 in astrocytoma. Further bioinformatics analysis indicated that miR‐124‐3p targeted the 3′‐ UTR of PIM 1. We also observed an inverse correlation between the miR‐124‐3p levels and PIM 1 protein or mRNA levels in astrocytoma samples. Next, we experimentally confirmed that miR‐124‐3p directly recognizes the 3′‐ UTR of the PIM 1 transcript and regulates PIM 1 expression at both the protein and mRNA levels. Furthermore, we examined the biological consequences of miR‐124‐3p targeting PIM 1 in vitro . We showed that the repression of PIM 1 in astrocytoma cancer cells by miR‐124‐3p suppressed proliferation, invasion, and aerobic glycolysis and promoted apoptosis. We observed that the restoration or inhibition of PIM 1 activity resulted in effects that were similar to those induced by miR‐124‐3p inhibitors or mimics in cancer cells. Finally, overexpression of PIM 1 rescued the inhibitory effects of miR‐124‐3p. In summary, these findings aid in understanding the tumor‐suppressive role of miR‐124‐3p in astrocytoma pathogenesis through the inhibition of PIM 1 translation.