ArticleJournal of experimental & clinical cancer research : CR2018
FAK-ERK activation in cell/matrix adhesion induced by the loss of apolipoprotein E stimulates the malignant progression of ovarian cancer.
Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
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- Locus- and Gene-Level Insights into the Inverse Association Between Alzheimer's Disease and Cancer.International journal of molecular sciences · 2026Article
- Regulation of Cell Proliferation and Migration by Extracellular Phosphatidic Acid.Biomedicines · 2026Review
- Rictor orchestrates β-catenin/FOXO balance by maintaining redox homeostasis during development of ovarian cancer.Oncogene · 2025Article
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- Identification of Quercetin as a Natural MMP1 Inhibitor for Overcoming Cisplatin Resistance in Epithelial Ovarian Cancer.Journal of Cancer · 2025Article
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- FAK-LINC01089 negative regulatory loop controls chemoresistance and progression of small cell lung cancer.Oncogene · 2024Article
- ZDHHC5-mediated S-palmitoylation of FAK promotes its membrane localization and epithelial-mesenchymal transition in glioma.Cell communication and signaling : CCS · 2024Article
- Identification of key genes associated with endometriosis and endometrial cancer by bioinformatics analysis.Frontiers in oncology · 2024Article
- Jun-APOE-LRP1 axis promotes tumor metastasis in colorectal cancer.Biomolecules & biomedicine · 2023Article
- Polygenic Propensity for Longevity, APOE-ε4 Status, Dementia Diagnosis, and Risk for Cause-Specific Mortality: A Large Population-Based Longitudinal Study of Older Adults.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023Article
- SEMA6C: a novel adhesion-independent FAK and YAP activator, required for cancer cell viability and growth.Cellular and molecular life sciences : CMLS · 2023Article
- Pin1/YAP pathway mediates matrix stiffness-induced epithelial-mesenchymal transition driving cervical cancer metastasis via a non-Hippo mechanism.Bioengineering & translational medicine · 2023Article
- Glycosylation and its research progress in endometrial cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Apolipoproteins: New players in cancers.Frontiers in pharmacology · 2022Review
- Ethanolic extract ofFrontiers in pharmacology · 2022Article
- FAK PROTAC Inhibits Ovarian Tumor Growth and Metastasis by Disrupting Kinase Dependent and Independent Pathways.Frontiers in oncology · 2022Article
- The Role of ApoE Expression and Variability of Its Glycosylation in Human Reproductive Health in the Light of Current Information.International journal of molecular sciences · 2021Review
- Upregulated Expression of CYBRD1 Predicts Poor Prognosis of Patients with Ovarian Cancer.Journal of oncology · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundExtracellular matrix (ECM) is a mediator of tumor progression. However, whether the alterations of the intraperitoneal ECM prior to tumor establishment affects the malignant progression of ovarian cancer remains elusive.
methodsApolipoprotein (ApoE) knock-out mice was used to analyze the intraperitoneal ECM alterations by quantification of the major components of ECM. ID8 cells were implanted in vivo to generate allografts and human ovarian cancer cell lines were characterized in vitro to assess the effects of ECM alterations on the malignant progression of ovarian cancer. Adhesion assay, immunochemistry, cytokines profile, proliferation assay, transwell invasion assay and western blot were used to determine the malignant phenotype of ovarian cancer cells.
resultsApoE loss induced increased ECM deposition, which stimulated the adhesions of ovarian cancer cells. The adhesion-mediated focal adhesion kinase (FAK) signaling enhanced the invasive behaviors of ovarian cancer cells through activation of a ERK-MMP linkage. This ECM-induced signaling cascade was further confirmed in human ovarian cancer cell lines in vitro. Furthermore, reversal of the ECM accumulation with BAPN or abrogation of adhesion-induced ERK activation in ovarian cancer cells with MEK inhibitors (MEKi) was found to effectively delay ovarian cancer progression.
conclusionsThese findings identify the FAK-ERK activation in cell/matrix adhesion in the malignant progression of ovarian cancer and the efficiency of BAPN or MEKi for tumor suppression, providing an impetus for further studies to explore the possibility of new anticancer therapeutic combinations.
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