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Tytuł pozycji:

Silencing PROK2 Inhibits Invasion of Human Cervical Cancer Cells by Targeting MMP15 Expression.

Tytuł :
Silencing PROK2 Inhibits Invasion of Human Cervical Cancer Cells by Targeting MMP15 Expression.
Autorzy :
Wu MH; Laboratory Department, Chung-Kang Branch, Cheng-Ching General Hospital, Taichung 40764, Taiwan.; Department of Medicinal Botanicals and Health Applications, Da-Yeh University, Chunghua 51591, Taiwan.
Wu PR; Department of Pathology, Cheng-Ching General Hospital, Taichung 40764, Taiwan.
Hsieh YH; Institute of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.
Lin CL; Institute of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.
Liu CJ; Division of Gastroenterology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung 80708, Taiwan.; Regenerative Medicine and Cell Therapy Research Center, Kaohsiung Medical University, Kaohsiung 80708, Taiwan.
Ying TH; Department of Obstetrics and Gynecology, Chung Shan Medical University Hospital, Taichung 40201, Taiwan.; Department of Obstetrics and Gynecology, School of Medicine, College of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.
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Źródło :
International journal of molecular sciences [Int J Mol Sci] 2020 Sep 02; Vol. 21 (17). Date of Electronic Publication: 2020 Sep 02.
Typ publikacji :
Journal Article
Język :
English
Imprint Name(s) :
Original Publication: Basel, Switzerland : MDPI, [2000-
MeSH Terms :
Gene Expression Regulation, Neoplastic*
Biomarkers, Tumor/*metabolism
Gastrointestinal Hormones/*metabolism
Matrix Metalloproteinase 15/*metabolism
Neuropeptides/*metabolism
Uterine Cervical Neoplasms/*pathology
Apoptosis ; Biomarkers, Tumor/genetics ; Cell Cycle ; Cell Movement ; Cell Proliferation ; Female ; Gastrointestinal Hormones/antagonists & inhibitors ; Gastrointestinal Hormones/genetics ; Humans ; Matrix Metalloproteinase 15/chemistry ; Matrix Metalloproteinase 15/genetics ; Neoplasm Invasiveness ; Neuropeptides/antagonists & inhibitors ; Neuropeptides/genetics ; Prognosis ; Tumor Cells, Cultured ; Uterine Cervical Neoplasms/genetics ; Uterine Cervical Neoplasms/metabolism
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Grant Information :
CH10800234A Chung-Kang Branch, Cheng-Ching General Hospital Research Fund; CSH-2020-D-008 Chung Shan Medical University Hospital; (KMUH108-8M02 Kaohsiung Medical University Hospital; KMU-TC108A02-2, KMU-TC108A02-4 Kaohsiung Medical University Research Center Grant
Contributed Indexing :
Keywords: MMP15; PROK2; cervical cancer; invasion; migration
Substance Nomenclature :
0 (Biomarkers, Tumor)
0 (Gastrointestinal Hormones)
0 (MMP15 protein, human)
0 (Neuropeptides)
0 (PROK2 protein, human)
EC 3.4.24.- (Matrix Metalloproteinase 15)
Entry Date(s) :
Date Created: 20200905 Date Completed: 20210325 Latest Revision: 20210325
Update Code :
20210326
PubMed Central ID :
PMC7504693
DOI :
10.3390/ijms21176391
PMID :
32887509
Czasopismo naukowe
Cervical cancer is the second most frequent type of gynecologic cancer worldwide. Prokineticin 2 (PROK2) is reported to be involved in tumor progression in some malignant tumors. However, the role of PROK2 in the development of cervical cancer remains unknown. Our results indicate that PROK2 is overexpressed in the human cervical cancer. Cervical cancer patients with high PROK2 expression have a shorter overall survival rate (OS) and disease-free survival rate (DFS). PROK2 acts as a potential biomarker for predicting OS and DFS of cervical cancer patients. We further show that PROK2 is important factor for oncogenic migration and invasion in human cervical cancer cells. Knockdown PROK2 significantly inhibited cell migration, invasion, and MMP15 protein expression in HeLa cells. High expression of MMP15 is confirmed in the human cervical cancer, is significantly associated with the shorter overall survival rate (OS) and is correlated with PROK2 expression. Overexpression of PROK2 using PROK2 plasmid significantly reverses the function of knockdown PROK2, and further upregulates MMP15 expression, migration and invasion of human cervical cancer cells. In conclusion, our findings are the first to demonstrate the role of PROK2 as a novel and potential biomarker for clinical use, and reveal the oncogenic functions of PROK2 as therapeutic target for cervical cancer.

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