PMID- 33168027
OWN - NLM
STAT- MEDLINE
DCOM- 20210804
LR  - 20230929
IS  - 1756-9966 (Electronic)
IS  - 0392-9078 (Print)
IS  - 0392-9078 (Linking)
VI  - 39
IP  - 1
DP  - 2020 Nov 9
TI  - LncRNA MYLK-AS1 facilitates tumor progression and angiogenesis by targeting 
      miR-424-5p/E2F7 axis and activating VEGFR-2 signaling pathway in hepatocellular 
      carcinoma.
PG  - 235
LID - 10.1186/s13046-020-01739-z [doi]
LID - 235
AB  - BACKGROUND: Long non-coding RNAs (lncRNAs) are crucial in the invasion, 
      angiogenesis, progression, and metastasis of hepatocellular carcinoma (HCC). The 
      lncRNA MYLK-AS1 promotes the growth and invasion of HCC through the 
      EGFR/HER2-ERK1/2 signaling pathway. However, the clinical significance of 
      MYLK-AS1 in HCC still needs to be further determined. METHODS: Bioinformatic 
      analysis was performed to determine the potential relationship among MYLK-AS1, 
      miRNAs and mRNAs. A total of 156 samples of normal liver and paired HCC tissues 
      from HCC patients were used to evaluate MYLK-AS1 expression by qRT-PCR. Human HCC 
      cell lines were used to evaluate the colony formation, cell proliferation, 
      migration, invasion, cell cycle and apoptosis after transfection of lentiviral 
      short-hairpin RNAs (shRNAs) targeting MYLK-AS1 or MYLK-AS1 vectors. The 
      competitive endogenous RNA (ceRNA) mechanism was clarified using fluorescence in 
      situ hybridization (FISH), Western blotting, qPCR, RNA binding protein 
      immunoprecipitation (RIP), and dual luciferase reporter analysis. RESULTS: 
      MYLK-AS1 up-regulation was detected in the HCC tumor tissues and cell lines 
      associated with the enhancement of the angiogenesis and tumor progression. The 
      down-regulation of MYLK-AS1 reversed the effects on angiogenesis, proliferation, 
      invasion and metastasis in the HCC cells and in vivo. MYLK-AS1 acted as ceRNA, 
      capable of regulating the angiogenesis in HCC, while the microRNA miR-424-5p was 
      the direct target of MYLK-AS1. Promoting the angiogenesis and the tumor 
      proliferation, the complex MYLK-AS1/miR-424-5p activated the VEGFR-2 signaling 
      through E2F7, whereas the specific targeting of E2F transcription factor 7 (E2F7) 
      by miR-424-5p, was indicated by the mechanism studies. CONCLUSIONS: MYLK-AS1 and 
      E2F7 are closely related to some malignant clinicopathological features and 
      prognosis of HCC, thus the MYLK-AS1/ miR-424-5p/E2F7 signaling pathway might 
      represent a promising treatment strategy to combat HCC.
FAU - Teng, Fei
AU  - Teng F
AD  - Department of Hepatobiliary and Pancreatic Surgery, Minhang Hospital, Fudan 
      University, Shanghai, 201199, People's Republic of China.
AD  - Institute of Fudan-Minhang Academic Health System, Minhang Hospital, Fudan 
      University, Shanghai, 201199, People's Republic of China.
FAU - Zhang, Ju-Xiang
AU  - Zhang JX
AD  - Shanghai Med-X Engineering Center for Medical Equipment and Technology, School of 
      Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, 200030, People's 
      Republic of China.
FAU - Chang, Qi-Meng
AU  - Chang QM
AD  - Department of Hepatobiliary and Pancreatic Surgery, Minhang Hospital, Fudan 
      University, Shanghai, 201199, People's Republic of China.
AD  - Institute of Fudan-Minhang Academic Health System, Minhang Hospital, Fudan 
      University, Shanghai, 201199, People's Republic of China.
FAU - Wu, Xu-Bo
AU  - Wu XB
AD  - Department of Hepatobiliary and Pancreatic Surgery, Minhang Hospital, Fudan 
      University, Shanghai, 201199, People's Republic of China.
AD  - Institute of Fudan-Minhang Academic Health System, Minhang Hospital, Fudan 
      University, Shanghai, 201199, People's Republic of China.
FAU - Tang, Wei-Guo
AU  - Tang WG
AD  - Department of Hepatobiliary and Pancreatic Surgery, Minhang Hospital, Fudan 
      University, Shanghai, 201199, People's Republic of China.
AD  - Institute of Fudan-Minhang Academic Health System, Minhang Hospital, Fudan 
      University, Shanghai, 201199, People's Republic of China.
FAU - Wang, Jian-Fa
AU  - Wang JF
AD  - Department of Hepatobiliary and Pancreatic Surgery, Minhang Hospital, Fudan 
      University, Shanghai, 201199, People's Republic of China.
AD  - Institute of Fudan-Minhang Academic Health System, Minhang Hospital, Fudan 
      University, Shanghai, 201199, People's Republic of China.
FAU - Feng, Jin-Feng
AU  - Feng JF
AD  - Department of Hepatobiliary and Pancreatic Surgery, Minhang Hospital, Fudan 
      University, Shanghai, 201199, People's Republic of China.
AD  - Institute of Fudan-Minhang Academic Health System, Minhang Hospital, Fudan 
      University, Shanghai, 201199, People's Republic of China.
FAU - Zhang, Zi-Ping
AU  - Zhang ZP
AD  - Department of Hepatobiliary and Pancreatic Surgery, Minhang Hospital, Fudan 
      University, Shanghai, 201199, People's Republic of China. zhang_zp@fudan.edu.cn.
AD  - Institute of Fudan-Minhang Academic Health System, Minhang Hospital, Fudan 
      University, Shanghai, 201199, People's Republic of China. zhang_zp@fudan.edu.cn.
FAU - Hu, Zhi-Qiu
AU  - Hu ZQ
AUID- ORCID: 0000-0002-3244-1607
AD  - Department of Hepatobiliary and Pancreatic Surgery, Minhang Hospital, Fudan 
      University, Shanghai, 201199, People's Republic of China. huzq@fudan.edu.cn.
AD  - Institute of Fudan-Minhang Academic Health System, Minhang Hospital, Fudan 
      University, Shanghai, 201199, People's Republic of China. huzq@fudan.edu.cn.
LA  - eng
GR  - 2019MHZ079/Shanghai Minhang Science and Technology Commission (CN)/
GR  - 2019MHJC04/Fundamental Medical Project of Minhang Hospital of Fudan University 
      Project Foundation/
PT  - Journal Article
DEP - 20201109
PL  - England
TA  - J Exp Clin Cancer Res
JT  - Journal of experimental & clinical cancer research : CR
JID - 8308647
RN  - 0 (Calcium-Binding Proteins)
RN  - 0 (E2F7 Transcription Factor)
RN  - 0 (E2F7 protein, human)
RN  - 0 (MIRN424 microrna, human)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Antisense)
RN  - 0 (RNA, Long Noncoding)
RN  - EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-2)
RN  - EC 2.7.11.18 (MYLK protein, human)
RN  - EC 2.7.11.18 (Myosin-Light-Chain Kinase)
SB  - IM
EIN - J Exp Clin Cancer Res. 2020 Dec 9;39(1):277. PMID: 33298087
EIN - J Exp Clin Cancer Res. 2023 Sep 30;42(1):257. PMID: 37775828
MH  - Calcium-Binding Proteins/*genetics
MH  - Carcinoma, Hepatocellular/*blood supply/genetics/metabolism/pathology
MH  - Disease Progression
MH  - E2F7 Transcription Factor/*metabolism
MH  - Female
MH  - Humans
MH  - Liver Neoplasms/*blood supply/genetics/metabolism/pathology
MH  - Male
MH  - MicroRNAs/*metabolism
MH  - Middle Aged
MH  - Myosin-Light-Chain Kinase/*genetics
MH  - Neovascularization, Pathologic/genetics/metabolism/pathology
MH  - Prognosis
MH  - RNA, Antisense/genetics/metabolism
MH  - RNA, Long Noncoding/*metabolism
MH  - Signal Transduction
MH  - Transfection
MH  - Vascular Endothelial Growth Factor Receptor-2/*metabolism
PMC - PMC7650167
OTO - NOTNLM
OT  - Competing endogenous RNA
OT  - E2F7
OT  - Hepatocellular carcinoma
OT  - Long non-coding RNAs, MYLK-AS1
OT  - VEGFR-2, miR-424-5p
COIS- The authors declare that they have no competing interests.
EDAT- 2020/11/11 06:00
MHDA- 2021/08/05 06:00
PMCR- 2020/11/09
CRDT- 2020/11/10 05:32
PHST- 2020/08/29 00:00 [received]
PHST- 2020/10/14 00:00 [accepted]
PHST- 2020/11/10 05:32 [entrez]
PHST- 2020/11/11 06:00 [pubmed]
PHST- 2021/08/05 06:00 [medline]
PHST- 2020/11/09 00:00 [pmc-release]
AID - 10.1186/s13046-020-01739-z [pii]
AID - 1739 [pii]
AID - 10.1186/s13046-020-01739-z [doi]
PST - epublish
SO  - J Exp Clin Cancer Res. 2020 Nov 9;39(1):235. doi: 10.1186/s13046-020-01739-z.