ArticleScientific reports2017
Unconventional MAPK-GSK-3β Pathway Behind Atypical Epithelial-Mesenchymal Transition In Hepatocellular Carcinoma.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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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
1 citing paper in PubMed, 5 citations in OpenAlex.
- Ribosomal protein L22-like1 (RPL22L1) mediates sorafenib sensitivity via ERK in hepatocellular carcinoma.Cell death discovery · 2022Article
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
We recently reported an atypical epithelial mesenchymal transition (EMT) in human hepatoma cell culture Huh7.5, which was non-responsive to the canonical EMT-transcription factors. Here we characterize major pathways regulating this atypical EMT through whole genome transcriptome profiling and molecular analysis, and identify a unique regulation of EMT by GSK-3β. Our analysis reveals remarkable suppression of several key liver-specific markers in Huh7.5M cells indicating that EMT not only changes the epithelial properties, but alters the characteristics associated with hepatocytes as well. One key finding of this study is that GSK-3β, a known antagonist to β-Catenin signaling and a major pro-apoptotic regulator, is critical for the maintenance of EMT in Huh7.5M cells as its inhibition reversed EMT. Importantly, through these studies we identify that maintenance of EMT by GSK-3β in Huh7.5M is regulated by p38MAPK and ERK1/2 that has not been reported elsewhere and is distinct from another metastatic non-hepatic cell line MDA-MB-231. These data showcase the existence of non-canonical mechanisms behind EMT. The atypicalness of this system underlines the existence of tremendous diversity in cancer-EMT and warrants the necessity to take a measured approach while dealing with metastasis and cancer drug resistance.
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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.