PMID- 29138865
OWN - NLM
STAT- MEDLINE
DCOM- 20180720
LR  - 20190404
IS  - 1791-2431 (Electronic)
IS  - 1021-335X (Linking)
VI  - 39
IP  - 1
DP  - 2018 Jan
TI  - Silencing of vacuolar ATPase c subunit ATP6V0C inhibits the invasion of prostate 
      cancer cells through a LASS2/TMSG1-independent manner.
PG  - 298-306
LID - 10.3892/or.2017.6092 [doi]
AB  - Vacuolar ATPase (V-ATPase), widespread in eukaryotic cells, is extensively
      expressed in many highly metastatic tumors, of which the V-ATPase c subunit
      ATP6V0C is particularly associated with the invasion and metastasis of cancer.
      ATP6V0C was directly found to interact with LASS2/TMSG1 which is a new tumor
      metastasis inhibitory gene identified by our laboratory in 1999. In order to
      study the role of ATP6V0C, we generated small interference RNA (siRNA) targeting 
      ATP6V0C and investigated its function on the invasion of human prostate cancer
      cell line PC-3M-1E8 with high metastatic potential and its interplay with
      LASS2/TMSG1. We found that the expression of ATP6V0C was higher in prostate
      cancer cell lines PC-3M-1E8 and PC-3M with high metastatic potential than that
      from cell lines PC-3M-2B4 and PC-3 with low metastatic potential, indicating that
      ATP6V0C enhanced metastatic capacity in prostate cancer cells. Furthermore,
      silencing of ATP6V0C in PC-3M-1E8 cells inhibited V-ATPase activity (by ~5-fold),
      decreased extracellular hydrogen ion concentration and successively decreased
      activation of secreted MMP-9 (by ~3.6-fold), which coincided with the inhibition 
      of cell migration and invasion in vitro, as well as a marked decrease in the
      expression of LASS2/TMSG1 probably through positive feedback. Thus we concluded
      that silencing of the ATP6V0C gene effectively suppressed the migration and
      invasion of prostate carcinoma cells through the inhibition of the function of
      V-ATPase, not through a LASS2/TMSG1-dependent manner. Therefore ATP6V0C
      inhibitors are promising therapeutic targets for advanced prostate cancer.
FAU - Zou, Pengcheng
AU  - Zou P
AD  - Department of Pathology, School of Basic Medical Sciences, Peking University
      Health Science Center, Beijing 100191, P.R. China.
FAU - Yang, Yifeng
AU  - Yang Y
AD  - Department of Pathology, School of Basic Medical Sciences, Peking University
      Health Science Center, Beijing 100191, P.R. China.
FAU - Xu, Xiaoyan
AU  - Xu X
AD  - Department of Pathology, School of Basic Medical Sciences, Peking University
      Health Science Center, Beijing 100191, P.R. China.
FAU - Liu, Beiying
AU  - Liu B
AD  - School of Mechanical Engineering, University of Science and Technology Beijing,
      Beijing 100191, P.R. China.
FAU - Mei, Fang
AU  - Mei F
AD  - Department of Pathology, School of Basic Medical Sciences, Peking University
      Health Science Center, Beijing 100191, P.R. China.
FAU - You, Jiangfeng
AU  - You J
AD  - Department of Pathology, School of Basic Medical Sciences, Peking University
      Health Science Center, Beijing 100191, P.R. China.
FAU - Liu, Qichen
AU  - Liu Q
AD  - Yuxin School of Capital Normal University, Beijing 100048, P.R. China.
FAU - Pei, Fei
AU  - Pei F
AD  - Department of Pathology, School of Basic Medical Sciences, Peking University
      Health Science Center, Beijing 100191, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20171110
PL  - Greece
TA  - Oncol Rep
JT  - Oncology reports
JID - 9422756
RN  - 0 (ATP6V0C protein, human)
RN  - 0 (Membrane Proteins)
RN  - 0 (Tumor Suppressor Proteins)
RN  - EC 2.3.1.24 (CERS2 protein, human)
RN  - EC 2.3.1.24 (Sphingosine N-Acyltransferase)
RN  - EC 3.4.24.35 (MMP9 protein, human)
RN  - EC 3.4.24.35 (Matrix Metalloproteinase 9)
RN  - EC 3.6.1.- (Vacuolar Proton-Translocating ATPases)
SB  - IM
MH  - Cell Line, Tumor
MH  - Cell Movement
MH  - Feedback, Physiological
MH  - Gene Expression Regulation, Neoplastic
MH  - Gene Knockdown Techniques/*methods
MH  - Humans
MH  - Male
MH  - Matrix Metalloproteinase 9/metabolism
MH  - Membrane Proteins/genetics/*metabolism
MH  - Neoplasm Invasiveness
MH  - Prostatic Neoplasms/*genetics/metabolism/pathology
MH  - Sphingosine N-Acyltransferase/genetics/*metabolism
MH  - Tumor Suppressor Proteins/genetics/*metabolism
MH  - Up-Regulation
MH  - Vacuolar Proton-Translocating ATPases/*genetics/metabolism
EDAT- 2017/11/16 06:00
MHDA- 2018/07/22 06:00
CRDT- 2017/11/16 06:00
PHST- 2017/02/13 00:00 [received]
PHST- 2017/08/01 00:00 [accepted]
PHST- 2017/11/16 06:00 [pubmed]
PHST- 2018/07/22 06:00 [medline]
PHST- 2017/11/16 06:00 [entrez]
AID - 10.3892/or.2017.6092 [doi]
PST - ppublish
SO  - Oncol Rep. 2018 Jan;39(1):298-306. doi: 10.3892/or.2017.6092. Epub 2017 Nov 10.