ArticleAmerican journal of cancer research2014
Expression of migfilin is increased in esophageal cancer and represses the Akt-β-catenin activation.
Article in American journal of cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Migfilin promotes autophagic flux through direct interaction with SNAP29 and Vamp8.The Journal of cell biology · 2024Article
- Integrative analyses of bulk and single-cell RNA-seq identified cancer-associated fibroblasts-related signature as a prognostic factor for immunotherapy in NSCLC.Cancer immunology, immunotherapy : CII · 2023Article
- circFBLIM1 act as a ceRNA to promote hepatocellular cancer progression by sponging miR-346.Journal of experimental & clinical cancer research : CR · 2018Article
- Regulation of XIAP Turnover Reveals a Role for USP11 in Promotion of Tumorigenesis.EBioMedicine · 2017Article
- MicroRNA-182 drives colonization and macroscopic metastasis via targeting its suppressor SNAI1 in breast cancer.Oncotarget · 2017Article
- Regulation of β-catenin-mediated esophageal cancer growth and invasion by miR-214.American journal of translational research · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell adhesion proteins that connect each cell to neighboring cells and the extracellular matrix are an important determinant of cell morphology and metastasis. Migfilin is a member of LIM-containing protein family, mediated the linkage between cytoskeleton and focal adhesion through interacting with other proteins and involved in cell adhesion and motility. The present study used immunohistochemistry and Western blot analysis of migfilin in clinical specimens of esophageal squamous cell carcinoma (ESCC) to identify that the expression of migfilin was significantly upregulated in ESCC in concomitance with a nuclear-cytoplasm translocation compared to normal adjacent tissue. Alternately, using the published datasets we identified that the expression of β-catenin was upregulated in esophageal cancer cells with focal invasion, while inversely correlated with migfilin in esophageal cancer cell lines. We demonstrated that the reduced expression of β-catenin by migfilin was through the inhibition of Akt activation. In conclusion, these results illustrated that migfilin upregulated in ESCCs and repressed β-catenin in an Akt-GSK3β signaling dependent manner.
Indexed as
Identifiers
24959381PMC4065407W266123765What 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.