ArticleMolecular medicine reports2018
FAK regulates epithelial‑mesenchymal transition in adenomyosis.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- The interaction between inflammation and estrogen in adenomyosis : from molecular mechanisms to therapeutic strategies.Seminars in immunopathology · 2026Review
- Mechanistic insights into inflammatory cytokines in adenomyosis‑induced infertility (Review).International journal of molecular medicine · 2026Review
- Focal adhesion kinase promotes biphasic differentiation and induces infiltration and metastasis of synovial sarcoma.Journal of translational medicine · 2026Article
- Genome-wide profiling of salivary promoter-region DNA methylation in periodontitis: the Tromsø Study.BMC medical genomics · 2026Article
- Polydopamine-Coated Surfaces Promote Adhesion, Migration, Proliferation, Chemoresistance, Stemness, and Epithelial-Mesenchymal Transition of Human Prostate Cancer Cell Lines In Vitro via Integrin αInternational journal of molecular sciences · 2026Article
- Strictosamide and mitraphylline inhibit cancer cell motility by suppressing epithelial-mesenchymal transition via integrin α4-mediated signaling.Scientific reports · 2025Article
- ATF4/NUPR1 axis promotes cancer cell survival and mediates immunosuppression in clear cell renal cell carcinoma.Discover oncology · 2024Article
- T-plastin contributes to epithelial-mesenchymal transition in human lung cancer cells through FAK/AKT/Slug axis signaling pathway.BMB reports · 2024Article
- The small protein LINC01547-ORF inhibits colorectal cancer progression by regulating the CLDN18-FAK-AKT axis.American journal of cancer research · 2024Article
- Morphological and cytoskeleton changes in cells after EMT.Scientific reports · 2023Article
- Pancreatic ductal adenocarcinoma: tumor microenvironment and problems in the development of novel therapeutic strategies.Clinical and experimental medicine · 2023Review
- MIR503HG silencing promotes endometrial stromal cell progression and metastasis and suppresses apoptosis in adenomyosis by activating the Wnt/β‑catenin pathway via targeting miR‑191.Experimental and therapeutic medicine · 2023Article
- Cycloartocarpin Inhibits Migration through the Suppression of Epithelial-to-Mesenchymal Transition and FAK/AKT Signaling in Non-Small-Cell Lung Cancer Cells.Molecules (Basel, Switzerland) · 2022Article
- RNA-seq reveals co-dysregulated circular RNAs in the adenomyosis eutopic endometrium and endometrial-myometrial interface.BMC women's health · 2022Article
- The Role of mTOR and eIF Signaling in Benign Endometrial Diseases.International journal of molecular sciences · 2022Review
- FAK in Cancer: From Mechanisms to Therapeutic Strategies.International journal of molecular sciences · 2022Review
- Mechanism Study of Cinnamomi Ramulus andEvidence-based complementary and alternative medicine : eCAM · 2022Article
- Origin and Pathogenic Mechanisms of Uterine Adenomyosis: What Is Known So Far.Reproductive sciences (Thousand Oaks, Calif.) · 2021Review
- Upregulated Talin1 synergistically boosts β-estradiol-induced proliferation and pro-angiogenesis of eutopic and ectopic endometrial stromal cells in adenomyosis.Reproductive biology and endocrinology : RB&E · 2021Article
- Artocarpin Targets Focal Adhesion Kinase-Dependent Epithelial to Mesenchymal Transition and Suppresses Migratory-Associated Integrins in Lung Cancer Cells.Pharmaceutics · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial‑mesenchymal transition (EMT) has been associated with the pathogenesis of adenomyosis; focal adhesion kinase (FAK) serves an important role in the EMT process. The aim of the present study was to determine whether FAK regulates EMT in adenomyosis and to investigate the potential pathway in this process. The expression of FAK and EMT‑associated molecules in adenomyosis and control cells were determined by immunohistochemical staining and immunofluorescence at the protein level, and at the mRNA level by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). Small interfering RNAs were designed to knock down FAK expression. Subsequently, molecular expression was detected by immunofluorescence, RT‑qPCR and western blotting; cell migration was investigated via Transwell assays. In addition, the expression levels of members of the phosphoinositide 3‑kinase (PI3K)/protein kinase B (AKT) signaling pathway was also analyzed by RT‑qPCR and western blotting to determine the association between these members and EMT in adenomyosis. The results of the present study revealed that FAK was upregulated and the expression levels of EMT‑associated molecules were altered in adenomyosis. Silencing FAK expression inhibited adenomyosis cell migration in vitro and the expression of EMT‑promoting molecules, suggesting that the FAK/PI3K/AKT signaling pathway may participate in the EMT of endometrial cells in adenomyosis. In conclusion, FAK may regulate EMT in adenomyosis, and this process may be associated with the PI3K/AKT signaling pathway.
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