Transforming growth factor β1 (TGF-β1) plays an important role in tumor initiation and development by inducing epithelial-mesenchymal Transition (EMT). Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) is a long noncoding RNA (lncRNA) that contributes to the invasion and metastasis of tumors, including esophageal squamous cell carcinoma (ESCC). The aim of the present study was to explore the underlying mechanisms implicated in EMT and to clarify whether TGF-β1 regulates MALAT1 expression, thereby promoting the invasion of ESCC. Expression of TGF-β1, MALAT1 and EMT-related markers, including E-cadherin and Vimentin, was detected in clinical samples of Kazakh's ESCC. The role of TGF-β1 in the regulation of MALAT1 in ESCC invasion was evaluated at the ESCC cell line level. High TGF-β1 expression was significantly associated with poor survival among patients with Kazakh's ESCC. Additionally, the expression of Vimentin was upregulated, and the expression of E-cadherin was downregulated and varied. The expression of MALAT1 positively correlated with the expression of TGF-β1 both and . Furthermore, knockdown of MALAT1 inhibited TGF-β1-induced EMT. Our data indicate that MALAT1 is heavily involved in EMT induced by TGF-β1. MALAT1 may be a therapeutic target in the suppression of metastasis and invasion of ESCC.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7592017 | PMC |
http://dx.doi.org/10.7150/jca.48426 | DOI Listing |
Cells
January 2025
School of Medicine, Newgiza University (NGU), Giza 12577, Egypt.
Meis1 is a transcription factor involved in numerous functions including development and proliferation and has been previously shown to harness cell cycle progression. In this study, we used in silico analysis to predict that miR-499-5p targets Meis1 and that Malat1 sponges miR-499-5p. For the first time, we demonstrated that the overexpression of miR-499-5p led to the downregulation of Meis1 mRNA and protein in C166 cells by directly binding to its 3'UTR.
View Article and Find Full Text PDFJ Oral Biol Craniofac Res
January 2025
Centre of Molecular Medicine and Diagnostics (COMManD), Department of Biochemistry, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai, 600077, India.
Objective: This study explores the role of MALAT1 as a valuable target for creating minimally-invasive diagnostic methods and personalized treatments in the management of OSCC. It focuses on evaluating the role of exosomal MALAT1 in the progression of dysplasia to OSCC by influencing the PI3K/AKT pathway.
Method: This cross-sectional study evaluated MALAT1 expression and PI3K/AKT pathway components in exosomes derived from plasma samples of patients with various stages of oral dysplasia, OSCC and compared with normal.
Proteomes
January 2025
Instituto de Matemática e Estatística, Departamento de Ciência da Computação, Universidade de São Paulo, Rua do Matão 1010, São Paulo 05508-090, SP, Brazil.
The tumor suppressor p53, in its wild-type form, plays a central role in cellular homeostasis by regulating senescence, apoptosis, and autophagy within the DNA damage response (DDR). Recent findings suggest that wild-type p53 also governs ferroptosis, an iron-dependent cell death process driven by lipid peroxidation. Post-translational modifications of p53 generate proteoforms that significantly enhance its functional diversity in regulating these mechanisms.
View Article and Find Full Text PDFWorld J Gastroenterol
January 2025
Department of Oncology Surgery, Cell Therapy and Organ Transplantation, Institute of Biomedicine of Seville, Virgen del Rocio University Hospital, Seville 41013, Spain.
Background: Hepatocellular carcinoma (HCC) is the most common subtype of primary liver cancer with varied incidence and epidemiology worldwide. Sorafenib is still a recommended treatment for a large proportion of patients with advanced HCC. Different patterns of treatment responsiveness have been identified in differentiated hepatoblastoma HepG2 cells and metastatic HCC SNU449 cells.
View Article and Find Full Text PDFJ Biol Chem
January 2025
Department of Chemistry and Biochemistry, University of California San Diego, La Jolla, CA 92093, USA. Electronic address:
TAR DNA-binding protein (TDP-43) and Metastasis Associated Lung Adenocarcinoma Transcript (MALAT1) RNA are both abundantly expressed in the human cell nucleus. Increased interaction of TDP-43 and MALAT1, as well as dysregulation of TDP-43 function, was previously identified in brain samples from patients with neurodegenerative disease compared to healthy brain tissues. We hypothesized that TDP-43 function may depend in part on MALAT1 expression levels.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!