PMID- 29449553
OWN - NLM
STAT- MEDLINE
DCOM- 20200406
LR  - 20220330
IS  - 2041-4889 (Electronic)
VI  - 9
IP  - 3
DP  - 2018 Feb 15
TI  - Nuclear factor 90 promotes angiogenesis by regulating HIF-1alpha/VEGF-A expression 
      through the PI3K/Akt signaling pathway in human cervical cancer.
PG  - 276
LID - 10.1038/s41419-018-0334-2 [doi]
LID - 276
AB  - Vascular endothelial growth factor A (VEGF-A), a fundamental component of 
      angiogenesis, provides nutrients and oxygen to solid tumors, and enhances tumor 
      cell survival, invasion, and migration. Nuclear factor 90 (NF90), a 
      double-stranded RNA-binding protein, is strongly expressed in several human 
      cancers, promotes tumor growth by reducing apoptosis, and increasing cell cycle 
      process. The mechanisms by which cervical cancer cells inducing VEGF-A expression 
      and angiogenesis upon NF90 upregulation remain to be fully established. We 
      demonstrated that NF90 is upregulated in human cervical cancer specimens and the 
      expression of NF90 is paralleled with that of VEGF-A under hypoxia. The 
      expressions of hypoxia inducible factor-1alpha (HIF-1alpha) and VEGF-A are downregulated 
      upon NF90 knockdown, which can be rescued by ectopic expression of NF90. 
      Suppression of NF90 decreases the tube formation and cell migration of HUVECs. 
      Moreover, the PI3K/Akt signaling pathway participates in the regulation. 
      Knockdown of NF90 also reduces the tumor growth and angiogenesis of cervical 
      cancer cell line in the mouse xenograft model. Taken together, suppression of 
      NF90 in cervical cancer cell lines can decrease VEGF-A expression, inhibit 
      angiogenesis, and reduce tumorigenic capacity in vivo.
FAU - Zhang, Wenqian
AU  - Zhang W
AD  - Department of Obstetrics and Gynecology, The Second Affiliated Hospital, 
      Chongqing Medical University, 400010, Chongqing, China.
FAU - Xiong, Zhengai
AU  - Xiong Z
AD  - Department of Obstetrics and Gynecology, The Second Affiliated Hospital, 
      Chongqing Medical University, 400010, Chongqing, China. xza20171022@sina.com.
FAU - Wei, Tianqin
AU  - Wei T
AD  - Department of Obstetrics and Gynecology, The Second Affiliated Hospital, 
      Chongqing Medical University, 400010, Chongqing, China.
FAU - Li, Qiumeng
AU  - Li Q
AD  - Department of Neurosurgery, The Second Affiliated Hospital, Chongqing Medical 
      University, 400010, Chongqing, China.
FAU - Tan, Ying
AU  - Tan Y
AD  - Department of Neurosurgery, The Second Affiliated Hospital, Chongqing Medical 
      University, 400010, Chongqing, China.
FAU - Ling, Li
AU  - Ling L
AD  - Department of Obstetrics and Gynecology, The Second Affiliated Hospital, 
      Chongqing Medical University, 400010, Chongqing, China.
FAU - Feng, Xiushan
AU  - Feng X
AD  - Department of Obstetrics and Gynecology, The Second Affiliated Hospital, 
      Chongqing Medical University, 400010, Chongqing, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180215
PL  - England
TA  - Cell Death Dis
JT  - Cell death & disease
JID - 101524092
RN  - 0 (HIF1A protein, human)
RN  - 0 (Hypoxia-Inducible Factor 1, alpha Subunit)
RN  - 0 (ILF3 protein, human)
RN  - 0 (Nuclear Factor 90 Proteins)
RN  - 0 (VEGFA protein, human)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - EC 2.7.1.137 (Phosphatidylinositol 3-Kinase)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - Animals
MH  - Cell Movement
MH  - Cell Proliferation
MH  - Female
MH  - Gene Expression Regulation, Neoplastic
MH  - HeLa Cells
MH  - Human Umbilical Vein Endothelial Cells/enzymology
MH  - Humans
MH  - Hypoxia-Inducible Factor 1, alpha Subunit/genetics/*metabolism
MH  - Mice, Inbred BALB C
MH  - Mice, Nude
MH  - *Neovascularization, Pathologic
MH  - Nuclear Factor 90 Proteins/genetics/*metabolism
MH  - Phosphatidylinositol 3-Kinase/*metabolism
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - Signal Transduction
MH  - Tumor Burden
MH  - Uterine Cervical Neoplasms/*blood supply/*enzymology/pathology
MH  - Vascular Endothelial Growth Factor A/genetics/*metabolism
PMC - PMC5833414
COIS- The authors declare that they have no conflict of interest.
EDAT- 2018/02/17 06:00
MHDA- 2020/04/09 06:00
PMCR- 2018/02/15
CRDT- 2018/02/17 06:00
PHST- 2017/10/29 00:00 [received]
PHST- 2018/01/19 00:00 [accepted]
PHST- 2018/01/17 00:00 [revised]
PHST- 2018/02/17 06:00 [entrez]
PHST- 2018/02/17 06:00 [pubmed]
PHST- 2020/04/09 06:00 [medline]
PHST- 2018/02/15 00:00 [pmc-release]
AID - 10.1038/s41419-018-0334-2 [pii]
AID - 334 [pii]
AID - 10.1038/s41419-018-0334-2 [doi]
PST - epublish
SO  - Cell Death Dis. 2018 Feb 15;9(3):276. doi: 10.1038/s41419-018-0334-2.