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Decreased expression of TCF12 contributes to progression and predicts biochemical recurrence in patients with prostate cancer.

Abstract As a member of helix-loop-helix protein family, transcription factor 12 functions as either an oncogene or a tumor suppressor in various human cancers. However, there are no reports on its involvement in prostate cancer. To investigate clinical relevance of transcription factor 12 in prostate cancer and to evaluate its roles in malignant phenotypes of this cancer in vitro and in vivo, we here examined expression patterns of transcription factor 12 protein in 50 prostate cancer tissue specimens by immunohistochemistry. Then, associations of transcription factor 12 expression with various clinicopathological characteristics and patients' prognosis of prostate cancer were evaluated. Its involvements in cancer cell proliferation, migration, invasion, and tumor growth were determined by in vitro and in vivo experiments. As a result, the positive immunostaining of transcription factor 12 protein was localized in cytoplasm and/or nucleus of prostate cancer cells. Its expression levels were decreased with prostate cancer Gleason score increased. Statistically, the decreased expression of transcription factor 12 protein more frequently occurred in prostate cancer patients with high Gleason score, positive metastasis, prostate-specific antigen failure, and short biochemical recurrence-free survival (all p < 0.05). Importantly, multivariate analysis showed that the status of transcription factor 12 expression was an independent predictor of biochemical recurrence-free survival in prostate cancer. Functionally, enforced expression of transcription factor 12 suppressed cell proliferation, migration, and invasion in vitro and inhibited tumor growth in vivo. In conclusion, transcription factor 12 protein may be a novel molecule which plays a critical role in prostate cancer progression and patients' prognosis, suggesting it might be a promising therapeutic target for prostate cancer therapy.
PMID
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Authors

Mayor MeshTerms
Keywords

Transcription factor 12

biochemical recurrence

clinicopathological characteristics

malignant phenotype

prostate cancer

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




PMID- 28651494
OWN - NLM
STAT- MEDLINE
DA  - 20170627
DCOM- 20170710
LR  - 20170713
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 6
DP  - 2017 Jun
TI  - Decreased expression of TCF12 contributes to progression and predicts biochemical
      recurrence in patients with prostate cancer.
PG  - 1010428317703924
LID - 10.1177/1010428317703924 [doi]
AB  - As a member of helix-loop-helix protein family, transcription factor 12 functions
      as either an oncogene or a tumor suppressor in various human cancers. However,
      there are no reports on its involvement in prostate cancer. To investigate
      clinical relevance of transcription factor 12 in prostate cancer and to evaluate 
      its roles in malignant phenotypes of this cancer in vitro and in vivo, we here
      examined expression patterns of transcription factor 12 protein in 50 prostate
      cancer tissue specimens by immunohistochemistry. Then, associations of
      transcription factor 12 expression with various clinicopathological
      characteristics and patients' prognosis of prostate cancer were evaluated. Its
      involvements in cancer cell proliferation, migration, invasion, and tumor growth 
      were determined by in vitro and in vivo experiments. As a result, the positive
      immunostaining of transcription factor 12 protein was localized in cytoplasm
      and/or nucleus of prostate cancer cells. Its expression levels were decreased
      with prostate cancer Gleason score increased. Statistically, the decreased
      expression of transcription factor 12 protein more frequently occurred in
      prostate cancer patients with high Gleason score, positive metastasis,
      prostate-specific antigen failure, and short biochemical recurrence-free survival
      (all p &lt; 0.05). Importantly, multivariate analysis showed that the status of
      transcription factor 12 expression was an independent predictor of biochemical
      recurrence-free survival in prostate cancer. Functionally, enforced expression of
      transcription factor 12 suppressed cell proliferation, migration, and invasion in
      vitro and inhibited tumor growth in vivo. In conclusion, transcription factor 12 
      protein may be a novel molecule which plays a critical role in prostate cancer
      progression and patients' prognosis, suggesting it might be a promising
      therapeutic target for prostate cancer therapy.
FAU - Chen, Qing-Biao
AU  - Chen QB
AD  - 1 Affiliated Foshan Hospital of Southern Medical University, Southern Medical
      University, Foshan, China.
AD  - 2 Department of Urology, Huadu District People's Hospital, Southern Medical
      University, Guangzhou, China.
FAU - Liang, Ying-Ke
AU  - Liang YK
AD  - 3 Department of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine 
      and Diagnostics, Guangzhou First People's Hospital, Guangzhou Medical University,
      Guangzhou, China.
FAU - Zhang, Yan-Qiong
AU  - Zhang YQ
AD  - 4 China Institute of Chinese Materia Medica, China Academy of Chinese Medical
      Sciences, Beijing, China.
FAU - Jiang, Min-Yao
AU  - Jiang MY
AD  - 2 Department of Urology, Huadu District People's Hospital, Southern Medical
      University, Guangzhou, China.
FAU - Han, Zhao-Dong
AU  - Han ZD
AD  - 3 Department of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine 
      and Diagnostics, Guangzhou First People's Hospital, Guangzhou Medical University,
      Guangzhou, China.
FAU - Liang, Yu-Xiang
AU  - Liang YX
AD  - 3 Department of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine 
      and Diagnostics, Guangzhou First People's Hospital, Guangzhou Medical University,
      Guangzhou, China.
FAU - Wan, Yue-Ping
AU  - Wan YP
AD  - 2 Department of Urology, Huadu District People's Hospital, Southern Medical
      University, Guangzhou, China.
FAU - Yin, Jie
AU  - Yin J
AD  - 1 Affiliated Foshan Hospital of Southern Medical University, Southern Medical
      University, Foshan, China.
FAU - He, Hui-Chan
AU  - He HC
AD  - 5 Urology Key Laboratory of Guangdong Province, The First Affiliated Hospital of 
      Guangzhou Medical University, Guangzhou Medical University, Guangzhou, China.
FAU - Zhong, Wei-de
AU  - Zhong WD
AD  - 2 Department of Urology, Huadu District People's Hospital, Southern Medical
      University, Guangzhou, China.
AD  - 3 Department of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine 
      and Diagnostics, Guangzhou First People's Hospital, Guangzhou Medical University,
      Guangzhou, China.
AD  - 5 Urology Key Laboratory of Guangdong Province, The First Affiliated Hospital of 
      Guangzhou Medical University, Guangzhou Medical University, Guangzhou, 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 (Basic Helix-Loop-Helix Transcription Factors)
RN  - 0 (Biomarkers, Tumor)
RN  - 142661-93-6 (TCF12 protein, human)
RN  - EC 3.4.21.77 (Prostate-Specific Antigen)
SB  - IM
MH  - Aged
MH  - Basic Helix-Loop-Helix Transcription Factors/biosynthesis/*genetics
MH  - Biomarkers, Tumor/biosynthesis/*genetics
MH  - Cell Proliferation/genetics
MH  - Disease Progression
MH  - Disease-Free Survival
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Neoplasm Grading
MH  - Neoplasm Recurrence, Local/*genetics/pathology
MH  - Prostate-Specific Antigen/blood
MH  - Prostatic Neoplasms/blood/*genetics/pathology
OTO - NOTNLM
OT  - Transcription factor 12
OT  - biochemical recurrence
OT  - clinicopathological characteristics
OT  - malignant phenotype
OT  - prostate cancer
EDAT- 2017/06/28 06:00
MHDA- 2017/07/14 06:00
CRDT- 2017/06/28 06:00
AID - 10.1177/1010428317703924 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Jun;39(6):1010428317703924. doi: 10.1177/1010428317703924.