Knockdown of Ubiquitin Associated Protein 2-Like (UBAP2L) Inhibits Growth and Metastasis of Hepatocellular Carcinoma.
Med Sci Monit
; 24: 7109-7118, 2018 Oct 06.
Article
in En
| MEDLINE
| ID: mdl-30291221
ABSTRACT
BACKGROUND The aim of this study was to explore the influence of ubiquitin associated protein 2-like (UBAP2L) on the growth and metastasis of hepatocellular carcinoma (HCC) and its potential underlying mechanism. MATERIAL AND METHODS UBAP2L gene was knocked down in SMMC-7721 by RNA interference and cell function experiments were performed. A subcutaneous xenograft tumor model was constructed to examine the effect of UBAP2L silence on HCC growth. Finally, the whole genomic microarrays were used to screen the potential mechanism of UBAP2L in regulating the biological function of HCC. RESULTS Compared with those in the control group, the cell proliferation and clone formation were significantly reduced, cell cycle was arrested in G2/M phase, the number of apoptotic cells was remarkably increased, and the abilities of vascular formation and cell migration and metastasis were dramatically weakened in the shUBAP2L group (All P<0.05). UBAP2L knockdown significantly suppressed the tumor growth of HCC in vivo. Moreover, a total of 320 genes changed significantly after UBAP2L knockdown, among which, 159 genes were upregulated and 161 genes were downregulated. Then, gene enrichment analysis revealed that PI3K/AKT and P53 signal pathway were the most significant in the top 10 enrichments. Finally, Western blot analysis verified that UBAP2L knockdown caused the increase of P21 and PTEN and decrease of CDK1, CCNB1, p-PI3K, and p-AKT. CONCLUSIONS UBAP2L plays an oncogenic role in HCC, and knockdown of its expression significantly inhibits HCC growth and metastasis, which may be related to the regulation of PI3K/AKT and P53 signaling pathways by UBAP2L.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Carrier Proteins
/
Carcinoma, Hepatocellular
/
Liver Neoplasms
Type of study:
Risk_factors_studies
Limits:
Humans
Language:
En
Journal:
Med Sci Monit
Journal subject:
MEDICINA
Year:
2018
Document type:
Article