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Overexpression of WDFY2 inhibits prostate cancer cell growth and migration via inactivation of Akt pathway.

Abstract Prostate cancer is the most commonly diagnosed malignancy and is the second leading deadly reason among male cancer. WDFY2, which is found to be a cancer-specific fusion gene with CDKN2D in ovarian cancer, is a new gene with unknown function in carcinogenesis. In this study, we investigated the role of WDFY2 in prostate cancer development. We examined WDFY2 expression in human prostate tissue specimens and prostate cancer cell lines BPH-1, LNCaP, PC3, and DU-145. Overexpression of WDFY2 was performed to evaluate the role of WDFY2 in cell proliferation, migration, and colony formation of prostate cancer cells. We analyzed the clinical impact and prognosis of WDFY2 expression on the progress of prostate cancer through data from online datasets. Our results showed that WDFY2 had lower expression level in prostate tumors than in normal tissues. Overexpression of WDFY2 in prostate cancer cells DU145 and PC-3 led to the suppression of cancer cell migration and colony formation. Furthermore, we found that WDFY2 exerted its role by suppressing the activity of Akt pathway other than the epithelial-mesenchymal transition progression. In conclusion, we have uncovered WDFY2 as a tumor suppressor gene and a new potential biomarker for cancer progression. Our results showed that WDFY2 inhibited cancer cell colony formation and migration via suppressing Akt pathway, making it a potential new therapeutic target in prostate cancer.
PMID
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Authors

Mayor MeshTerms
Keywords

Akt pathway

WDFY2

migration and colony formation

prostate cancer

Journal Title tumour biology : the journal of the international society for oncodevelopmental biology and medicine
Publication Year Start




PMID- 28653900
OWN - NLM
STAT- MEDLINE
DA  - 20170627
DCOM- 20170711
LR  - 20170713
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 6
DP  - 2017 Jun
TI  - Overexpression of WDFY2 inhibits prostate cancer cell growth and migration via
      inactivation of Akt pathway.
PG  - 1010428317704821
LID - 10.1177/1010428317704821 [doi]
AB  - Prostate cancer is the most commonly diagnosed malignancy and is the second
      leading deadly reason among male cancer. WDFY2, which is found to be a
      cancer-specific fusion gene with CDKN2D in ovarian cancer, is a new gene with
      unknown function in carcinogenesis. In this study, we investigated the role of
      WDFY2 in prostate cancer development. We examined WDFY2 expression in human
      prostate tissue specimens and prostate cancer cell lines BPH-1, LNCaP, PC3, and
      DU-145. Overexpression of WDFY2 was performed to evaluate the role of WDFY2 in
      cell proliferation, migration, and colony formation of prostate cancer cells. We 
      analyzed the clinical impact and prognosis of WDFY2 expression on the progress of
      prostate cancer through data from online datasets. Our results showed that WDFY2 
      had lower expression level in prostate tumors than in normal tissues.
      Overexpression of WDFY2 in prostate cancer cells DU145 and PC-3 led to the
      suppression of cancer cell migration and colony formation. Furthermore, we found 
      that WDFY2 exerted its role by suppressing the activity of Akt pathway other than
      the epithelial-mesenchymal transition progression. In conclusion, we have
      uncovered WDFY2 as a tumor suppressor gene and a new potential biomarker for
      cancer progression. Our results showed that WDFY2 inhibited cancer cell colony
      formation and migration via suppressing Akt pathway, making it a potential new
      therapeutic target in prostate cancer.
FAU - Wang, Jianqing
AU  - Wang J
AD  - 1 Department of Urology, Huashan Hospital, Fudan University, Shanghai, P.R.
      China.
FAU - Chen, Xu
AU  - Chen X
AD  - 2 Institutes of Biomedical Sciences, Fudan University, Shanghai, P.R. China.
FAU - Tong, Shijun
AU  - Tong S
AD  - 1 Department of Urology, Huashan Hospital, Fudan University, Shanghai, P.R.
      China.
FAU - Zhou, Huihui
AU  - Zhou H
AD  - 3 Department of Pathology, Affiliated Yuhuangding Hospital of Qingdao University,
      Qingdao, P.R. China.
FAU - Sun, Jianliang
AU  - Sun J
AD  - 1 Department of Urology, Huashan Hospital, Fudan University, Shanghai, P.R.
      China.
FAU - Gou, Yuancheng
AU  - Gou Y
AD  - 1 Department of Urology, Huashan Hospital, Fudan University, Shanghai, P.R.
      China.
FAU - Wu, Fei
AU  - Wu F
AD  - 1 Department of Urology, Huashan Hospital, Fudan University, Shanghai, P.R.
      China.
FAU - Hu, Jimeng
AU  - Hu J
AD  - 1 Department of Urology, Huashan Hospital, Fudan University, Shanghai, P.R.
      China.
FAU - Xu, Jianfeng
AU  - Xu J
AD  - 1 Department of Urology, Huashan Hospital, Fudan University, Shanghai, P.R.
      China.
AD  - 4 Program for Personalized Cancer Care and Department of Surgery, North Shore
      University Health System, Evanston, IL, USA.
FAU - Ding, Guanxiong
AU  - Ding G
AD  - 1 Department of Urology, Huashan Hospital, Fudan University, Shanghai, P.R.
      China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Tumour Biol
JT  - Tumour biology : the journal of the International Society for Oncodevelopmental
      Biology and Medicine
JID - 8409922
RN  - 0 (CDKN2D protein, human)
RN  - 0 (Cyclin-Dependent Kinase Inhibitor p19)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (WDFY2 protein, human)
SB  - IM
MH  - Aged
MH  - Carcinogenesis/genetics
MH  - Cell Line, Tumor
MH  - Cell Movement/genetics
MH  - Cell Proliferation/*genetics
MH  - Cyclin-Dependent Kinase Inhibitor p19/genetics
MH  - Epithelial-Mesenchymal Transition/*genetics
MH  - Female
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Intracellular Signaling Peptides and Proteins/biosynthesis/*genetics
MH  - Male
MH  - Middle Aged
MH  - Prognosis
MH  - Prostatic Neoplasms/*genetics/pathology
MH  - Signal Transduction
OTO - NOTNLM
OT  - Akt pathway
OT  - WDFY2
OT  - migration and colony formation
OT  - prostate cancer
EDAT- 2017/06/28 06:00
MHDA- 2017/07/14 06:00
CRDT- 2017/06/28 06:00
AID - 10.1177/1010428317704821 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Jun;39(6):1010428317704821. doi: 10.1177/1010428317704821.