During organogenesis, epithelial cells can give rise to mesenchymal cells through epithelial-mesenchymal transition. The reverse process, mesenchymal-epithelial transition (MET), can similarly generate epithelial cells. Transitions between epithelial and mesenchymal states are also critical for the induction of pluripotent stem cells from somatic cells. This Review discusses the relatively less characterized process of MET, focusing on the genesis of apicobasal cell polarity and exploring the roles of MET in development and reprogramming.
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http://dx.doi.org/10.1038/s41556-018-0195-z | DOI Listing |
Acta Pharmacol Sin
January 2025
State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious diseases, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China.
Cancer heterogeneity, characterized by diverse populations of tumorigenic cells, involves the occurrence of differential phenotypes with variable expressions of receptor tyrosine kinases. Aberrant expressions of mesenchymal-epithelial transition (MET) and recepteur d'origine nantais (RON) receptors contribute to the phenotypic heterogeneity of cancer cells, which poses a major therapeutic challenge. This study aims to develop a dual-targeting antibody-drug conjugate (ADC) that can act against both MET and RON for treating cancers with high phenotypic heterogeneity.
View Article and Find Full Text PDFJ Exp Clin Cancer Res
January 2025
Microenvironment and Biomarkers of Solid Tumors Unit, Department of Experimental Oncology, Amadeolab Fondazione IRCCS Istituto Nazionale Dei Tumori Di Milano, Milan, Italy.
Background: Growing evidence shows that the reprogramming of fatty acid (FA) metabolism plays a key role in HER2-positive (HER2 +) breast cancer (BC) aggressiveness, therapy resistance and cancer stemness. In particular, HER2 + BC has been defined as a "lipogenic disease" due to the functional and bi-directional crosstalk occurring between HER2-mediated oncogenic signaling and FA biosynthesis via FA synthase activity. In this context, the functional role exerted by the reprogramming of CD36-mediated FA uptake in HER2 + BC poor prognosis and therapy resistance remains unclear.
View Article and Find Full Text PDFAdv Exp Med Biol
January 2025
Lester and Sue Smith Breast Center, Houston, TX, USA.
This chapter reviews tumor-associated myeloid cells, including macrophages, neutrophils, and other innate immune cells, and their multifaceted roles in supporting breast cancer progression and metastasis. In primary tumors, myeloid cells play key roles in promoting tumor epithelial-mesenchymal transition (EMT) and invasion. They can facilitate intravasation (entry into the bloodstream) and colonization, disrupting the endothelial cell layer and reshaping the extracellular matrix.
View Article and Find Full Text PDFAnticancer Agents Med Chem
January 2025
Experiment Center for Science and Technology, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Unlabelled: Mesenchymal‒epithelial transition factor (c-Met), a receptortyrosine kinase (RTK), plays a vital role in cell proliferation, migration and invasion, and tumour metastasis.
Objective: With increasing duration of treatment, many tumours gradually develop drug resistance. Therefore, novel antitumour drugs need to be developed to treat patients with tumours.
Zhongguo Fei Ai Za Zhi
November 2024
Department of Oncology, The Central Hospital of Shaoyang, Shaoyang 422000, China.
With the rapid development of epidermal growth factor receptor (EGFR) gene testing of lung adenocarcinoma patients has been routinely carried out, EGFR mutations are also possible for some small samples of non-smoking female lung squamous cell carcinoma patients. This increases the opportunity for targeted therapy for this group of patients. However, drug resistance in patients with lung squamous cell carcinoma during targeted therapy is an important factor affecting subsequent treatment.
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