Cell migration is a multifactorial/multistep process that requires the concerted action of growth and transcriptional factors, motor proteins, extracellular matrix remodeling and proteases. In this review, we focus on the role of transcription factors modulating Epithelial-to-Mesenchymal Transition (EMT-TFs), a fundamental process supporting both physiological and pathological cell migration. These EMT-TFs (Snail1/2, Twist1/2 and Zeb1/2) are labile proteins which should be stabilized to initiate EMT and provide full migratory and invasive properties. We present here a family of enzymes, the deubiquitinases (DUBs) which have a crucial role in counteracting polyubiquitination and proteasomal degradation of EMT-TFs after their induction by TGFβ, inflammatory cytokines and hypoxia. We also describe the DUBs promoting the stabilization of Smads, TGFβ receptors and other key proteins involved in transduction pathways controlling EMT.
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http://dx.doi.org/10.1042/EBC20190022 | DOI Listing |
Zoological Lett
January 2025
National Institutes of Natural Sciences, Exploratory Research Center On Life and Living Systems (ExCELLS), National Institute for Basic Biology, Okazaki, Aichi, 444-8787, Japan.
In vertebrates, skeletal muscle comprises fast and slow fibers. Slow and fast muscle cells in fish are spatially segregated; slow muscle cells are located only in a superficial region, and comprise a small fraction of the total muscle cell mass. Slow muscles support low-speed, low-force movements, while fast muscles are responsible for high-speed, high-force movements.
View Article and Find Full Text PDFCancer Cell Int
January 2025
Department of Urology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Background: Tumor microenvironment (TME) plays a crucial role in tumor growth and metastasis. Exploring biomarkers that are significantly associated with TME can help guide individualized treatment of patients.
Methods: We analyzed the expression and survival of P4HB in pan-cancer through the TCGA database, and verified the protein level of P4HB by the HPA database.
Cancer Cell Int
January 2025
Department of Otolaryngology, Pudong Gongli Hospital, Shanghai, 200135, China.
Background: Specific molecular mechanisms by which AURKA promoted LSCC metastasis were still unknown.
Methods: Bioinformatic analysis was performed the relationship between TRIM28 and LSCC. Immunohistochemistry, Co-IP assay, Rt-PCR and Western Blot were used to examine the expression of related molecular.
Cell Commun Signal
January 2025
Centre of Postgraduate Medical Education, Centre of Translation Research, Department of Biochemistry and Molecular Biology, ul. Marymoncka 99/103, Warsaw, 01-813, Poland.
Background: Renal cell cancer (RCC) is the most common and highly malignant subtype of kidney cancer. Mesenchymal stromal cells (MSCs) are components of tumor microenvironment (TME) that influence RCC progression. The impact of RCC-secreted small non-coding RNAs (sncRNAs) on TME is largely underexplored.
View Article and Find Full Text PDFChin Med
January 2025
Department of Clinical Chinese Pharmacy, School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, 102488, China.
Background: With extended gefitinib treatment, the therapeutic effect in some non-small cell lung cancer (NSCLC) patients declined with the development of drug resistance. Aidi injection (ADI) is utilized in various cancers as a traditional Chinese medicine prescription. This study explores the molecular mechanism by which ADI, when combined with gefitinib, attenuates gefitinib resistance in PC9GR NSCLC cells.
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