PMID- 28078560
OWN - NLM
STAT- MEDLINE
DCOM- 20170316
LR  - 20231213
IS  - 1559-131X (Electronic)
IS  - 1357-0560 (Linking)
VI  - 34
IP  - 2
DP  - 2017 Feb
TI  - Knockdown of PYCR1 inhibits cell proliferation and colony formation via cell 
      cycle arrest and apoptosis in prostate cancer.
PG  - 27
LID - 10.1007/s12032-016-0870-5 [doi]
AB  - Pyrroline-5-carboxylate reductase 1 (PYCR1) is an enzyme involved in cell 
      metabolism, which has been shown to be up-regulated in cancers. However, the 
      functions of PYCR1 in prostate cancers (PCa) are still largely unknown. In the 
      present study, we found that PYCR1 was highly expressed in prostate cancer 
      tissues and then knocked down PYCR1 in PCa cell lines (DU145, PC-3 and LNCap) via 
      lentivirus-mediated gene delivery and analyzed its biological function. Both 
      qRT-PCR and western blotting indicated that PYCR1 was suppressed efficiently 
      after sh-PYCR1 infection. Further analysis indicated knockdown of PYCR1 
      significantly inhibited PCa cell growth and colony formation ability. The 
      inhibition effects on growth were likely due to G2/M-phase arrest and enhanced 
      cell apoptosis, as determined by flow cytometer analysis. At last, we verified 
      the expression levels of cell cycle regulatory proteins, including CDK1, CDK2, 
      CDK4 and Cyclin B1 were all downregulated and cell apoptotic-related proteins, 
      including cleaved caspase 3 and cleaved PARP were increased in PCa cells after 
      PYCR1 knockdown. Furthermore, PYCR1 has been shown not to be directly regulated 
      by androgen receptor (AR) levels. These results show the functions of PYCR1 in 
      PCa tumorigenesis for the first time and suggest that PYCR1 might be a good 
      potential therapy approach for treating PCa.
FAU - Zeng, Tengyue
AU  - Zeng T
AD  - Department of Urology, Fuzhou General Hospital, Fujian Medical University, 
      No.156, Xi'erhuan North Road, Fuzhou, 350025, China.
FAU - Zhu, Libing
AU  - Zhu L
AD  - Department of Urology, Lushan Sanatorium of the PLA, Lushan, 332000, China.
FAU - Liao, Min
AU  - Liao M
AD  - Department of Urology, Fuzhou General Hospital, Fujian Medical University, 
      No.156, Xi'erhuan North Road, Fuzhou, 350025, China.
FAU - Zhuo, Wenli
AU  - Zhuo W
AD  - Department of Urology, Fuzhou General Hospital, Fujian Medical University, 
      No.156, Xi'erhuan North Road, Fuzhou, 350025, China.
FAU - Yang, Shunliang
AU  - Yang S
AD  - Department of Urology, Fuzhou General Hospital, Fujian Medical University, 
      No.156, Xi'erhuan North Road, Fuzhou, 350025, China.
FAU - Wu, Weizhen
AU  - Wu W
AD  - Department of Urology, Fuzhou General Hospital, Fujian Medical University, 
      No.156, Xi'erhuan North Road, Fuzhou, 350025, China.
FAU - Wang, Dong
AU  - Wang D
AD  - Department of Urology, Fuzhou General Hospital, Fujian Medical University, 
      No.156, Xi'erhuan North Road, Fuzhou, 350025, China. wangdongdr@sina.com.
LA  - eng
PT  - Journal Article
DEP - 20170111
PL  - United States
TA  - Med Oncol
JT  - Medical oncology (Northwood, London, England)
JID - 9435512
RN  - 0 (AR protein, human)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Receptors, Androgen)
RN  - EC 1.5.1.- (Pyrroline Carboxylate Reductases)
SB  - IM
MH  - Apoptosis/physiology
MH  - Cell Line, Tumor
MH  - Cell Proliferation/physiology
MH  - G2 Phase Cell Cycle Checkpoints
MH  - Gene Knockdown Techniques
MH  - HEK293 Cells
MH  - Humans
MH  - M Phase Cell Cycle Checkpoints
MH  - Male
MH  - Middle Aged
MH  - Prostatic Neoplasms/*enzymology/genetics/metabolism/*pathology
MH  - Pyrroline Carboxylate Reductases/biosynthesis/genetics/*metabolism
MH  - RNA, Small Interfering/administration & dosage/genetics
MH  - Receptors, Androgen/metabolism
MH  - Signal Transduction
MH  - delta-1-Pyrroline-5-Carboxylate Reductase
OTO - NOTNLM
OT  - AR signaling
OT  - Apoptosis
OT  - Cell cycle
OT  - Cell proliferation
OT  - PYCR1
OT  - Prostate cancer
EDAT- 2017/01/13 06:00
MHDA- 2017/03/17 06:00
CRDT- 2017/01/13 06:00
PHST- 2015/07/16 00:00 [received]
PHST- 2016/12/19 00:00 [accepted]
PHST- 2017/01/13 06:00 [entrez]
PHST- 2017/01/13 06:00 [pubmed]
PHST- 2017/03/17 06:00 [medline]
AID - 10.1007/s12032-016-0870-5 [pii]
AID - 10.1007/s12032-016-0870-5 [doi]
PST - ppublish
SO  - Med Oncol. 2017 Feb;34(2):27. doi: 10.1007/s12032-016-0870-5. Epub 2017 Jan 11.