ArticleMolecular and cellular biochemistry2010
Focal adhesion kinase mediates TGF-beta1-induced renal tubular epithelial-to-mesenchymal transition in vitro.
Article in Molecular and cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 47 citations in OpenAlex.
- Focal adhesion kinase promotes biphasic differentiation and induces infiltration and metastasis of synovial sarcoma.Journal of translational medicine · 2026Article
- ADCY4 inhibits cAMP-induced growth of breast cancer by inactivating FAK/AKT and ERK signaling but is frequently silenced by DNA methylation.Scientific reports · 2025Article
- Single-cell transcriptomic analysis of gingivo-buccal oral cancer reveals two dominant cellular programs.Cancer science · 2023Article
- Knockdown of miR-214 Alleviates Renal Interstitial Fibrosis by Targeting the Regulation of the PTEN/PI3K/AKT Signalling Pathway.Oxidative medicine and cellular longevity · 2022Article
- A Luminacin D Analog HL142 Inhibits Ovarian Tumor Growth and Metastasis by Reversing EMT and Attenuating the TGFβ and FAK Pathways.Journal of Cancer · 2021Article
- Lin28a attenuates TGF-β-induced renal fibrosis.BMB reports · 2020Article
- Botulinum toxin type A prevents the phenotypic transformation of fibroblasts induced by TGF‑β1 via the PTEN/PI3K/Akt signaling pathway.International journal of molecular medicine · 2019Article
- Lysyl oxidase-like 2 is a regulator of angiogenesis through modulation of endothelial-to-mesenchymal transition.Journal of cellular physiology · 2019Article
- FAK regulates epithelial‑mesenchymal transition in adenomyosis.Molecular medicine reports · 2018Article
- 14, 15-EET induces breast cancer cell EMT and cisplatin resistance by up-regulating integrin αvβ3 and activating FAK/PI3K/AKT signaling.Journal of experimental & clinical cancer research : CR · 2018Article
- Targeting Src attenuates peritoneal fibrosis and inhibits the epithelial to mesenchymal transition.Oncotarget · 2017Article
- Negative feedback loop between ZBTB7A and TGF-β in breast cancer.Oncology letters · 2017Article
- Focal adhesion kinase signaling determines the fate of lung epithelial cells in response to TGF-β.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- AKT regulation of mesothelial-to-mesenchymal transition in peritoneal dialysis is modulated by Smurf2 and deubiquitinating enzyme USP4.BMC cell biology · 2015Article
- Article
- Dynamic Switch Between Two Adhesion Phenotypes in Colorectal Cancer Cells.Cellular and molecular bioengineering · 2014Article
- Erbin interacts with Sema4C and inhibits Sema4C-induced epithelial-mesenchymal transition in HK2 cells.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2013Article
- Suppression of SCARA5 by Snail1 is essential for EMT-associated cell migration of A549 cells.Oncogenesis · 2013Article
- IL-17 induces type V collagen overexpression and EMT via TGF-β-dependent pathways in obliterative bronchiolitis.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase which participates in many important cellular processes such as cell adhesion and migration. However, the role of FAK in renal tubular epithelial-to-mesenchymal transition (EMT) is still unknown. FAK was knocked down by transfection of specific small interfering RNA (siRNA) in cultured HK-2 cells, then the cells were stimulated with transforming growth factor-beta 1 (TGF-beta1). The expression of FAK, alpha-smooth muscle actin (alpha-SMA),E-cadherin, Akt, matrix metallopeptidase-9 (MMP-9),tissue inhibitor of metalloproteinase-1 (TIMP-1), and collagen IV were detected by RT-PCR, Western blot and immunofluorescence methods, respectively. Cell migration was determined by transwell assay. The results suggest that the expression of FAK was up-regulated in HK-2 cells when incubated with TGF-beta1(10 microg/l), which was accompanied by reduced expression of E-cadherin and increased expression of alpha-SMA. All these changes were restored by FAK siRNA. Akt phosphorylation was induced by the treatment with TGF-beta1, which was blocked by FAK siRNA. TGF-beta1-induced down-regulation of E-cadherin was recovered by a PI3K/Akt inhibitor, LY294002, without affecting the expression of FAK. Functionally, TGF-beta1 induced an increase in MMP-9 expression, as well as decreased expression of TIMP-1 and collagen IV, which were all restored by the FAK siRNA transfection. In addition, FAK siRNA significantly reduced TGF-beta1-induced cells migration. In conclusion, FAK may play a crucial role in mediating TGF-beta1-induced EMT through the activation of Akt pathway.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.