Background: Hyperthermia has been shown promising in the treatment of head and neck squamous cell carcinoma (HNSCC); however, the mechanism underlying hyperthermia reducing tumor metastasis is poorly elucidated. TWIST2, an important transcription factor of epithelial-mesenchymal transition (EMT), plays a critical role in the tumor progression and metastasis. The role of TWIST2 in tongue squamous cell carcinoma (TSCC) and its association with hyperthermia still have not been reported.
Method: The correlations between TWIST2 expression and the clinical-pathologic characteristics of 89 patients with TSCC were evaluated by immunohistochemical staining. TSCC cell lines transfected with siRNA against TWIST2 were heated for 40 min at 42.5°C, and the migration capability of cells was examined by migration assay. Xenograft tumors in nude mice were treated by hyperthermia, and TWIST2 expression was measured.
Results: Our data showed that TWIST2 expression was associated with the metastasis of human TSCC. In Tca8113 and Cal-27 cells, TWIST2-siRNA treatment can reduce cell migration ability and has no effect on the cell proliferation and apoptosis. Hyperthermia can decrease the level of TWIST2 in TSCC and inhibit the migration of cells.
Conclusions: This demonstrated that hyperthermia might decrease the migration of Tca8113 and Cal-27 cells by reducing TWIST2 expression. Altogether, these findings suggest an as yet undescribed link between TWIST2 and hyperthermia in TSCC.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/jop.12237 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Gene expression analysis reveals mir-29 as a linker regulatory molecule among rheumatoid arthritis, inflammatory bowel disease, and dementia: Insights from systems biology approach.
PLoS One
January 2025
Integrative Multiomics Lab, School of Bio Sciences and Technology, Vellore Institute of Technology, Vellore, Tamil Nadu, India.
Background: Rheumatoid arthritis (RA) is a degenerative autoimmune disease, often managed through symptomatic treatment. The co-occurrence of the reported extra-articular comorbidities such as inflammatory bowel disease (IBD), and dementia may complicate the pathology of the disease as well as the treatment strategies. Therefore, in our study, we aim to elucidate the key genes, and regulatory elements implicated in the progression and association of these diseases, thereby highlighting the linked potential therapeutic targets.
View Article and Find Full Text PDFComprehensive RNA Sequencing Analysis Identifies Network Hub Genes and Biomarkers Differentiating Desmoid-type Fibromatosis From Reactive Fibrosis.
Lab Invest
November 2024
Department of Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. Electronic address:
Article Synopsis
- Desmoid-type fibromatosis (DTF) is a benign but aggressive tumor caused by persistent activation of fibroblasts, differing from transient activation seen in reactive fibrosis (RF).
- A comparative analysis of gene expression in DTF and RF tissues revealed over 4,200 genes uniquely expressed in DTF, linked to development and muscle function, while RF genes pertained to immune responses.
- Key transcription factors associated with DTF were identified, and specific genes showed potential as biomarkers, with TWIST2 outperforming β-catenin as a diagnostic indicator for DTF.
Comparative Analysis of Transcription Factors TWIST2, GATA3, and HES5 in Glioblastoma Multiforme : Evaluating Biomarker Potential and Therapeutic Targets Using In Silico Methods.
J Korean Neurosurg Soc
October 2024
Department of Neurosurgery, Kangwon National University Hospital, Chuncheon, Korea.
Objective: Glioblastoma multiforme (GBM) is characterized by substantial heterogeneity and limited therapeutic options. As molecular approaches to central nervous system (CNS) tumors have gained prominence, this study examined the roles of three genes, TWIST2, GATA3, and HES5, known to be involved in oncogenesis, developmental processes, and maintenance of cancer stem cell properties, which have not yet been extensively studied in GBM. This study is the first to present gene expression data for TWIST2, GATA3, and HES5 specifically within the context of GBM patient survival.
View Article and Find Full Text PDFRelationship of Signaling Pathways between RKIP Expression and the Inhibition of EMT-Inducing Transcription Factors SNAIL1/2, TWIST1/2 and ZEB1/2.
Cancers (Basel)
September 2024
Department of Microbiology, Immunology & Molecular Genetics, David Geffen School of Medicine, Jonsson Comprehensive Cancer Center, University of California at Los Angeles, Los Angeles, CA 90095, USA.
Untreated primary carcinomas often lead to progression, invasion and metastasis, a process that involves the epithelial-to-mesenchymal transition (EMT). Several transcription factors (TFs) mediate the development of EMT, including SNAIL1/SNAIL2, TWIST1/TWIST2 and ZEB1/ZEB2, which are overexpressed in various carcinomas along with the under expression of the metastasis suppressor Raf Kinase Inhibitor Protein (RKIP). Overexpression of RKIP inhibits EMT and the above associated TFs.
View Article and Find Full Text PDFTargeting ITGβ3 to Overcome Trastuzumab Resistance through Epithelial-Mesenchymal Transition Regulation in HER2-Positive Breast Cancer.
Int J Mol Sci
August 2024
Department of Medical Biology, Faculty of Medicine, Karadeniz Technical University, Trabzon 61080, Turkey.
HER2-positive breast cancer, representing 15-20% of all breast cancer cases, often develops resistance to the HER2-targeted therapy trastuzumab. Unfortunately, effective treatments for advanced HER2-positive breast cancer remain scarce. This study aims to investigate the roles of ITGβ3, and Hedgehog signaling in trastuzumab resistance and explore the potential of combining trastuzumab with cilengitide as a therapeutic strategy.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!