Background/Aims:
A large number of differentially expressed molecules exist in hepatocellular carcinoma (HCC), and the mechanism by which they upregulate or downregulate expression is still unclear. The purpose of this study is to explore the possible mechanism of differential expression of apoptotic chromatin condensation inducer 1 (Acin1) in HCC.
Materials and Methods:
A mouse HCC model was constructed, and the expression of
Acin1
in HCC was analyzed by whole transcriptome sequencing, bioinformatics analysis, and reverse transcription-quantitative polymerase chain reaction, and differentially expressed
Acin1
-related genes were screened to construct a protein–protein interaction and competing endogenous RNA (ceRNA) network. The microRNA (miRNAs) targeting
Acin1
were further predicted using online databases and finally compared with sequencing data.
Results:
The expression of
Acin1
was significantly up-regulated in HCC compared to the paracancerous and healthy control groups (
P
< .001). The top 10 upregulated genes closely related to
Acin1
(
Slc3a2
,
Wiz
,
Srrm2
,
Akt1
,
Hnrnpu
,
Sap18b
,
Pabpn1
,
Ddx39b
,
Eif4a3
, and
Rnps1
) were mainly involved in pathways such as messenger RNA (mRNA) surveillance, RNA transport, spliceosome, Janus kinase/signal transducers and activators of transcription signaling, apoptosis, and ubiquitin-mediated proteolysis. The ceRNA network identified several molecules (2 long noncoding RNAs, 50 miRNAs, and 49 mRNAs) interacting with
Acin1
, among which miR-674-5p was highly expressed in all sample tissues, and higher than that of other differentially expressed miRNAs, and significantly downregulated in HCC. Multiple online databases such as miRWalk also predicted that miR-674-5p targets
Acin1
. This shows that miR-674-5p may be an important molecule for targeting
Acin1
.
Conclusion:
Acin1
is overexpressed in HCC, and the overexpressed
Acin1
is most likely regulated by miR-674-5p and other ceRNA molecules.