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Tytuł pozycji:

WNT6 participates in the occurrence and development of ovarian cancer by upregulating/activating the typical Wnt pathway and Notch1 signaling pathway.

Tytuł:
WNT6 participates in the occurrence and development of ovarian cancer by upregulating/activating the typical Wnt pathway and Notch1 signaling pathway.
Autorzy:
Bao H; Department of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou 510150, China.
Wu W; Department of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou 510150, China.
Li Y; Department of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou 510150, China.
Zong Z; Department of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou 510150, China; China Medical University, Shenyang 110001, China. Electronic address: zongzhi_.
Chen S; Department of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou 510150, China. Electronic address: .
Źródło:
Gene [Gene] 2022 Dec 20; Vol. 846, pp. 146871. Date of Electronic Publication: 2022 Sep 06.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Original Publication: Amsterdam, Elsevier/North-Holland, 1976-
MeSH Terms:
Ovarian Neoplasms*/metabolism
Wnt Signaling Pathway*
Apoptosis ; Carcinoma, Ovarian Epithelial/genetics ; Cell Line, Tumor ; Cell Proliferation ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; RNA, Messenger ; Receptor, Notch1/genetics ; Receptor, Notch1/metabolism ; Wnt Proteins/genetics ; Wnt Proteins/metabolism ; beta Catenin/genetics ; beta Catenin/metabolism
Contributed Indexing:
Keywords: Malignant tumors; Ovarian cancer; WNT signaling pathway; WNT6
Substance Nomenclature:
0 (NOTCH1 protein, human)
0 (RNA, Messenger)
0 (Receptor, Notch1)
0 (WNT6 protein, human)
0 (Wnt Proteins)
0 (beta Catenin)
Entry Date(s):
Date Created: 20220908 Date Completed: 20220928 Latest Revision: 20221004
Update Code:
20240104
DOI:
10.1016/j.gene.2022.146871
PMID:
36075327
Czasopismo naukowe
Wnt/β-catenin pathway is associated with the progression of various cancers such as gastric cancer, colorectal cancer, and endometrial cancer. Using the Kaplan-Meier Plotter database, we found that WNT6 was associated with progression-free survival (PFS) outcomes. Immunohistochemical analysis of ovarian cancer samples and normal ovaries showed that the expression of WNT6 protein was significantly increased in ovarian cancer samples. Further, we explored the possible role of WNT6 in the occurrence and development of ovarian cancer. Our results showed that the mRNA and protein expression of WNT6 were significantly higher in CAOV3 and OVCAR3 cells compared with other ovarian cancer cell lines and normal ovarian cell line IOSE-80 as well. The transformation of CAOV3 and OVCAR3 cells with short interfering WNT6 (siWNT6) significantly inhibited their proliferation and lamellipodia formation, causing cell cycle arrest and promoting cell apoptosis. Western blot experiments confirmed that the down-regulation of WNT6 inhibited the expression of β-catenin and Notch1. These results suggest that WNT6 plays an important role in the occurrence and development of ovarian cancer.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2022 Elsevier B.V. All rights reserved.)

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