FAM64A silencing inhibits the proliferation, migration, invasion, and epithelial-mesenchymal transition in ovarian cancer cells via activating Hippo pathway

Abstract Objective Ovarian cancer (OC) is a highly aggressive malignancy in females. We aim to investigate the potential gene target and examine its impact on OC. Methods Hub genes were determined using protein–protein interaction networks based on differently expressed genes in GSE12470 and GSE1440...

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Main Authors: Jianxiu Luo, Ruiyang Li
Format: Article
Language:English
Published: Springer 2025-06-01
Series:Discover Oncology
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Online Access:https://doi.org/10.1007/s12672-025-02710-0
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author Jianxiu Luo
Ruiyang Li
author_facet Jianxiu Luo
Ruiyang Li
author_sort Jianxiu Luo
collection DOAJ
description Abstract Objective Ovarian cancer (OC) is a highly aggressive malignancy in females. We aim to investigate the potential gene target and examine its impact on OC. Methods Hub genes were determined using protein–protein interaction networks based on differently expressed genes in GSE12470 and GSE14407 datasets. The impact of FAM64A on the malignant phenotype of OC cells was evaluated by cell counting kit-8, 5-ethynyl-2'-deoxyuridine staining, wound healing, and transwell assays. The epithelial-mesenchymal transition (EMT) process was assessed by determining the protein expression of E-cadherin, N-cadherin, and Vimentin. Results We identified the 18 hub genes of OC with substantial predictive value. FAM64A was selected as a candidate gene. The silencing of FAM64A suppressed the viability (si-NC: 0.78 ± 0.04, 0.95 ± 0.08; si-FAM64A: 0.58 ± 0.05, 0.64 ± 0.11), proliferation (si-NC: 100.00 ± 9.36, 100.00 ± 14.70; si-FAM64A: 34.79 ± 8.88, 44.55 ± 4.91), migration (si-NC: 61.92 ± 8.06, 60.08 ± 5.22; si-FAM64A: 45.88 ± 8.36, 37.78 ± 7.29), and invasion (si-NC: 130.00 ± 10.34, 144.00 ± 13.40; si-FAM64A: 81.00 ± 16.99, 115.60 ± 13.30) of A2780 and SKOV3 cells. FAM64A silencing reduced the EMT in OC cells. The Hippo pathway was identified as the central pathway implicated in the regulatory role of FAM64A in OC. The silencing of FAM64A caused an increase in the protein expression within the Hippo pathway in both A2780 and SKOV3 cells. Conclusion Knockdown of FAM64A emerges as a promising therapeutic target for OC, exerting an inhibitory role in OC by activating the Hippo pathway.
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spelling doaj-art-a886efe0946a44c3ae95abc384fad6db2025-08-20T03:47:13ZengSpringerDiscover Oncology2730-60112025-06-0116111510.1007/s12672-025-02710-0FAM64A silencing inhibits the proliferation, migration, invasion, and epithelial-mesenchymal transition in ovarian cancer cells via activating Hippo pathwayJianxiu Luo0Ruiyang Li1Department of Gynecology, Ganzhou People’s Hospital, Ganzhou Hospital-Nanfang Hospital, The Affiliated Ganzhou Hospital, Jiangxi Medical College, Southern Medical University, Nanchang UniversityDepartment of Oncology, The Third People’s Hospital of Jiujiang CityAbstract Objective Ovarian cancer (OC) is a highly aggressive malignancy in females. We aim to investigate the potential gene target and examine its impact on OC. Methods Hub genes were determined using protein–protein interaction networks based on differently expressed genes in GSE12470 and GSE14407 datasets. The impact of FAM64A on the malignant phenotype of OC cells was evaluated by cell counting kit-8, 5-ethynyl-2'-deoxyuridine staining, wound healing, and transwell assays. The epithelial-mesenchymal transition (EMT) process was assessed by determining the protein expression of E-cadherin, N-cadherin, and Vimentin. Results We identified the 18 hub genes of OC with substantial predictive value. FAM64A was selected as a candidate gene. The silencing of FAM64A suppressed the viability (si-NC: 0.78 ± 0.04, 0.95 ± 0.08; si-FAM64A: 0.58 ± 0.05, 0.64 ± 0.11), proliferation (si-NC: 100.00 ± 9.36, 100.00 ± 14.70; si-FAM64A: 34.79 ± 8.88, 44.55 ± 4.91), migration (si-NC: 61.92 ± 8.06, 60.08 ± 5.22; si-FAM64A: 45.88 ± 8.36, 37.78 ± 7.29), and invasion (si-NC: 130.00 ± 10.34, 144.00 ± 13.40; si-FAM64A: 81.00 ± 16.99, 115.60 ± 13.30) of A2780 and SKOV3 cells. FAM64A silencing reduced the EMT in OC cells. The Hippo pathway was identified as the central pathway implicated in the regulatory role of FAM64A in OC. The silencing of FAM64A caused an increase in the protein expression within the Hippo pathway in both A2780 and SKOV3 cells. Conclusion Knockdown of FAM64A emerges as a promising therapeutic target for OC, exerting an inhibitory role in OC by activating the Hippo pathway.https://doi.org/10.1007/s12672-025-02710-0FAM64AOvarian cancerHub genesHippo pathway
spellingShingle Jianxiu Luo
Ruiyang Li
FAM64A silencing inhibits the proliferation, migration, invasion, and epithelial-mesenchymal transition in ovarian cancer cells via activating Hippo pathway
Discover Oncology
FAM64A
Ovarian cancer
Hub genes
Hippo pathway
title FAM64A silencing inhibits the proliferation, migration, invasion, and epithelial-mesenchymal transition in ovarian cancer cells via activating Hippo pathway
title_full FAM64A silencing inhibits the proliferation, migration, invasion, and epithelial-mesenchymal transition in ovarian cancer cells via activating Hippo pathway
title_fullStr FAM64A silencing inhibits the proliferation, migration, invasion, and epithelial-mesenchymal transition in ovarian cancer cells via activating Hippo pathway
title_full_unstemmed FAM64A silencing inhibits the proliferation, migration, invasion, and epithelial-mesenchymal transition in ovarian cancer cells via activating Hippo pathway
title_short FAM64A silencing inhibits the proliferation, migration, invasion, and epithelial-mesenchymal transition in ovarian cancer cells via activating Hippo pathway
title_sort fam64a silencing inhibits the proliferation migration invasion and epithelial mesenchymal transition in ovarian cancer cells via activating hippo pathway
topic FAM64A
Ovarian cancer
Hub genes
Hippo pathway
url https://doi.org/10.1007/s12672-025-02710-0
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AT ruiyangli fam64asilencinginhibitstheproliferationmigrationinvasionandepithelialmesenchymaltransitioninovariancancercellsviaactivatinghippopathway