PMID- 30573973
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220330
IS  - 1178-6930 (Print)
IS  - 1178-6930 (Electronic)
IS  - 1178-6930 (Linking)
VI  - 11
DP  - 2018
TI  - Overexpressing lncRNA SNHG16 inhibited HCC proliferation and chemoresistance by 
      functionally sponging hsa-miR-93.
PG  - 8855-8863
LID - 10.2147/OTT.S182005 [doi]
AB  - BACKGROUND: Long noncoding RNAs (lncRNAs) have been identified as prognostic 
      biomarkers and functional regulators in human cancers. The present study aimed to 
      determine the expressions and functions of an lncRNA, Small Nucleolar RNA Host 
      Gene 16 (SNHG16), in hepatocellular carcinoma (HCC). PATIENTS AND METHODS: SNHG16 
      expressions were tested by quantitative real-time PCR (qRT-PCR) in HCC cell 
      lines, as well as 43 pairs of HCC tissues and pair-matched healthy hepatic 
      tissues. It was overexpressed in Hep3B and HuH7 cells. The effects of SNHG16 
      overexpression in HCC in vitro proliferation, 5-fluorouracil (5-FU) 
      chemoresistance, and in vivo tumor growth were tested. A potential microRNA 
      (miRNA) sponge target of SNHG16, hsa-miR-93, was tested by luciferase reporter 
      assay and qRT-PCR. In addition, hsa-miR-93 was upregulated in 
      SNHG16-overexpressed HCC cells to examine its effect on SNHG16-mediated cancer 
      cell functional regulation in HCC. RESULTS: SNHG16 levels were markedly 
      downregulated in both HCC cell lines and HCC tissues. Lentivirus-mediated SNHG16 
      overexpression inhibited HCC cell proliferation, 5-FU chemoresistance, and in 
      vivo tumor growth. Hsa-miR-93 was confirmed to be directly sponging on SNHG16. 
      Its upregulation in HCC cells reversed SNHG16 overexpression and induced 
      tumor-suppressing effects in HCC cells. CONCLUSION: Our data demonstrate that 
      SNHG16 plays a critical role in HCC development via functionally sponging 
      hsa-miR-93.
FAU - Xu, Fengfeng
AU  - Xu F
AD  - Department of General Surgery, The Fifth Affiliated Hospital of Guangzhou Medical 
      University, Guangzhou, People's Republic of China, ffxu555@aol.com.
FAU - Zha, Guoqing
AU  - Zha G
AD  - The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, People's 
      Republic of China.
FAU - Wu, Yanpeng
AU  - Wu Y
AD  - Department of General Surgery, The Fifth Affiliated Hospital of Guangzhou Medical 
      University, Guangzhou, People's Republic of China, ffxu555@aol.com.
FAU - Cai, Weilong
AU  - Cai W
AD  - Department of General Surgery, The Fifth Affiliated Hospital of Guangzhou Medical 
      University, Guangzhou, People's Republic of China, ffxu555@aol.com.
FAU - Ao, Jian
AU  - Ao J
AD  - Department of General Surgery, The Fifth Affiliated Hospital of Guangzhou Medical 
      University, Guangzhou, People's Republic of China, ffxu555@aol.com.
LA  - eng
PT  - Journal Article
DEP - 20181207
PL  - New Zealand
TA  - Onco Targets Ther
JT  - OncoTargets and therapy
JID - 101514322
PMC - PMC6290873
OTO - NOTNLM
OT  - SNHG16
OT  - hsa-miR-93
OT  - lncRNA
OT  - miRNA
OT  - proliferation
COIS- Disclosure The authors report no conflicts of interest in this work.
EDAT- 2018/12/24 06:00
MHDA- 2018/12/24 06:01
PMCR- 2018/12/07
CRDT- 2018/12/22 06:00
PHST- 2018/12/22 06:00 [entrez]
PHST- 2018/12/24 06:00 [pubmed]
PHST- 2018/12/24 06:01 [medline]
PHST- 2018/12/07 00:00 [pmc-release]
AID - ott-11-8855 [pii]
AID - 10.2147/OTT.S182005 [doi]
PST - epublish
SO  - Onco Targets Ther. 2018 Dec 7;11:8855-8863. doi: 10.2147/OTT.S182005. eCollection 
      2018.