PMID- 31427562
OWN - NLM
STAT- MEDLINE
DCOM- 20200214
LR  - 20211204
IS  - 1643-3750 (Electronic)
IS  - 1234-1010 (Print)
IS  - 1234-1010 (Linking)
VI  - 25
DP  - 2019 Aug 20
TI  - SOX18 Affects Cell Viability, Migration, Invasiveness, and Apoptosis in 
      Hepatocellular Carcinoma (HCC) Cells by Participating in 
      Epithelial-to-Mesenchymal Transition (EMT) Progression and Adenosine 
      Monophosphate Activated Protein Kinase (AMPK)/Mammalian Target of Rapamycin 
      (mTOR).
PG  - 6244-6254
LID - 10.12659/MSM.915729 [doi]
AB  - BACKGROUND Hepatocellular carcinoma (HCC) is one of the most common malignancies 
      around the world. It has been verified that the expression of SOX18 is correlated 
      to poor clinical prognosis in patients with ovarian cancer, non-small cell lung 
      cancer, or breast invasive ductal carcinoma. However, the expression pattern and 
      biological function of SOX18 in HCC tissues remains unclear. In this study, we 
      set out to investigate the associated biological function and potential molecular 
      mechanism of the SOX18 gene in HCC cells. MATERIAL AND METHODS The mRNA and 
      protein expression levels of experimental related genes were detected by 
      real-time polymerase chain reaction and western blotting assay, respectively. The 
      MTT method was used to assess cell viability, and cell apoptosis analysis was 
      performed by means of FACScan flow cytometry. Wound-healing assay and Transwell 
      analysis were performed to evaluate the ability of cell migration and 
      invasiveness, respectively. RESULTS SOX18 was highly expressed in various HCC 
      cell lines. In addition, SOX18 promoted cell viability, migration, and invasion 
      and simultaneously induce cell apoptosis. SOX18 promoted 
      epithelial-to-mesenchymal transition (EMT) progression, and SOX18 downregulation 
      activated the autophagy signaling pathway AMPK/mTOR in HCC cells. CONCLUSIONS 
      SOX18 downregulation in HCC cells suppressed cell viability and metastasis, 
      induced cell apoptosis and hindered the occurrence and progression of tumor cells 
      by participating in the EMT process and regulating the autophagy signaling 
      pathway AMPK/mTOR.
FAU - Sun, Yanni
AU  - Sun Y
AD  - Department of Hepatology, Yantai City Hospital for Infectious Diseases, Yantai, 
      Shandong, China (mainland).
FAU - Lei, Bo
AU  - Lei B
AD  - Department of Hepatology, Yantai City Hospital for Infectious Diseases, Yantai, 
      Shandong, China (mainland).
FAU - Huang, Qingxian
AU  - Huang Q
AD  - Department of Hepatobiliary Surgery, The Affiliated Yantai Yuhuangding Hospital 
      of Qingdao University, Yantai, Shandong, China (mainland).
LA  - eng
PT  - Journal Article
DEP - 20190820
PL  - United States
TA  - Med Sci Monit
JT  - Medical science monitor : international medical journal of experimental and 
      clinical research
JID - 9609063
RN  - 0 (SOX18 protein, human)
RN  - 0 (SOXF Transcription Factors)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.4.3 (Adenylate Kinase)
SB  - IM
MH  - Adenylate Kinase/*metabolism
MH  - Apoptosis/physiology
MH  - Carcinoma, Hepatocellular/genetics/*metabolism/*pathology
MH  - Cell Line, Tumor
MH  - Cell Movement/physiology
MH  - Cell Proliferation/physiology
MH  - Cell Survival/physiology
MH  - Epithelial-Mesenchymal Transition
MH  - Humans
MH  - Liver Neoplasms/genetics/*metabolism/*pathology
MH  - Neoplasm Invasiveness
MH  - SOXF Transcription Factors/*metabolism
MH  - Signal Transduction
MH  - TOR Serine-Threonine Kinases/*metabolism
PMC - PMC6713035
COIS- Conflict of interest None.
EDAT- 2019/08/21 06:00
MHDA- 2020/02/15 06:00
PMCR- 2019/08/20
CRDT- 2019/08/21 06:00
PHST- 2019/08/21 06:00 [entrez]
PHST- 2019/08/21 06:00 [pubmed]
PHST- 2020/02/15 06:00 [medline]
PHST- 2019/08/20 00:00 [pmc-release]
AID - 915729 [pii]
AID - 10.12659/MSM.915729 [doi]
PST - epublish
SO  - Med Sci Monit. 2019 Aug 20;25:6244-6254. doi: 10.12659/MSM.915729.