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Chemopreventive Agents
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Interestingly, the SNAIL signaling pathway triggers breast cancer metastasis but has no relevance in pancreatic cancer models. Also, EMT can be reversed via Mesenchymal-Epithelial Transition (MET) which is thought to facilitate the implanting of circulating tumor cells to develop secondary tumors when they reach a desirable target metastatic site. As part of this processes, the Extracellular Matrix (ECM) must be degraded, which is carried out by a proteolytic enzyme family, the Matrix Metalloproteinases (MMPs). These enzymes are key to tumor invasion, allowing tumor cells to degrade the ECM, penetrate the basement membrane, and move to other sites. MMPs also regulate cellular adhesion, which makes it easier for tumor cells to migrate. Cell Adhesion Molecules (CAMs) also play a significant role in tumor development and metastases, and include four groups: the Cadherins, Selectins, Integrins, and the Immunoglobulin Superfamily. A reduction or loss in Cadherin expression has been observed in some epithelial cancers, which is associated with increased invasion and metastasis. Activation of CAM proteins, including kinases and chemokines, can induce downstream signaling pathways, which ultimately promotes tumor growth and progression. Some chemopreventive agents are thought to work by inhibiting key regulators to suppress tumor invasion and metastasis.
Hereditary Papillary Renal Cell Cancer
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Hereditary papillary renal cell cancer (HPRCC) is an autosomal dominant genetic disorder characterized by the formation of multifocal or bilateral renal lesions with papillary type 1 morphology in patients of relatively young age (around 46 years). Molecularly, heterozygous germline mutations in the mesenchymal-epithelial transition factor gene (MET) on chromosome 7q31.2 underscore the tumorigenesis of HPRCC [1].
Ochratoxins
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Josué Delgado, Miguel A. Asensio, Félix Núñez
The development of cancer typically initiates with a mutated cell that begins to proliferate abnormally. Then, the cell proliferative stages of cancer involve the induction of signal transduction pathways that control the mitogenic effect triggering cell division. However, some toxicants operate through modifications that do not involve a change in the nucleotide sequence, but epigenetically control the gene expression leading to cancer. Information supporting DNA damage mediated by oxidative stress on the transcriptional level includes upregulation of calpactin I heavy chain, annexin V, and clusterin genes after OTA treatment.71 Deregulation of different signal transduction pathways can result in either cell division or cell death. The mitogen-activated protein kinases (MAPKs) have been shown to be strongly activated by OTA in canine renal tubular epithelial cells,72 in rat liver cells, and in human kidney cells.73–75 Different MAPK pathways, showing opposing effects, could be activated in dose- and time-dependent manners.74 As a result, an early and sustained activation of the MAPK/extracellular signal regulated kinase (Erk) pathway would lead to apoptosis, whereas a late activation of the mesenchymal epithelial transition factor (c-MET) pathway would promote carcinogenesis.
Pathology of breast cancer metastasis and a view of metastasis to the brain
Published in International Journal of Neuroscience, 2023
Md Sakibuzzaman, Shahriar Mahmud, Tanzina Afroze, Sawsan Fathma, Ummul Barakat Zakia, Sabrina Afroz, Farzina Zafar, Maksuda Hossain, Amit Barua, Sabiha Akter, Hasanul Islam Chowdhury, Eram Ahsan, Shayet Hossain Eshan, Tasnuva Tarannum Fariza
Two theories that contribute to brain metastases are mesenchymal-epithelial transition (MET) and partial MET. MET is the phenotypic reverse process of initial EMT occurring at the primary tumor site. During this process, the cancer cells re-express epithelial proteins, such as E-cadherin and pan-cytokeratin, and decrease the expression of mesenchymal proteins, such as N-cadherin [79,80]. This change enhances the survival of metastatic tumor cells in the microenvironment of secondary organs [80]. Yet, the contribution of MET in successful colonization is still under investigation [6]. BCCs maintain mesenchymal markers and enhance the expression of epithelial markers in partial MET [81]. This process allows cancer cells to colonize the brain by creating links with surrounding malignant cells via E-cadherin. For further metastasis into other cerebral areas, a second EMT happens.
Membrane Localization of β-Catenin in Prostate Cancer PC3 Cells Treated with Teucrium persicum Boiss. Extract
Published in Nutrition and Cancer, 2022
Narges Barati, Majid Tafrihi, S. Mahmoud A. Najafi
Our immunofluorescence experiments showed that T. persicum extract induced an epithelial-like phenotype in PC-3 cells. Non-treated PC-3 cells show a homogeneous cytoplasmic distribution for β-Catenin protein. Treatment of these cells with 10 and 25 µg/ml of T. persicum extract led to the formation of several patches of epithelial-like cells having β-Catenin at the cell membrane (Figure 2). This event is an important step in MET (mesenchymal-epithelial transition) process. The results of gene expression experiments showed a decrease in nuclear/transcriptional activities of β-Catenin in the cells treated with T. persicum extract. We chose three cellular β-Catenin-target genes including c-MYC, CCND1, and CDH1 plus a known reporter luciferase gene under the control of a few β-Catenin/TCF-responsive elements (TOPFlash) (39, 58, 59). It is worth mentioning that among the chosen cellular target genes, β-Catenin activity increases transcription of c-MYC and CCND1 while decreases the expression of CDH1 (37, 60).
The therapeutic efficacy and safety improvements of crizotinib prodrug micelles on breast cancer treatment
Published in Pharmaceutical Development and Technology, 2022
Yongjing Cao, Qiangwei Liang, Yang Lan, Yanhua Liu
Breast cancer is a malignant tumor with high morbidity and mortality and remains the leading cause of cancer death in women (Bray et al. 2018). Mesenchymal-epithelial transition factor (MET) is one most important elements in the development of breast cancer, which plays an important influence on the treatment tumor by mediating tumor growth, migration, invasion, angiogenesis, and resistance to targeted therapy. MET overexpression is characterized by poor prognosis in breast cancer, which is manifested by higher histological grade, larger tumor, more metastatic sites, and reduced recurrence-free survival rate (Shi et al. 2021). Met is a receptor tyrosine kinase (RTK) that upon binding of its ligand, hepatocyte growth factor (HGF), activates downstream pathways with diverse cellular functions, which influences breast cancer growth, invasion, and metastasis (Ho-Yen et al. 2015). In addition, Cro remains a multi-target tyrosine kinase inhibitor targeting anaplastic lymphoma kinase (ALK) gene recombination, MET gene amplification and ROS gene (Comoglio et al. 2018). Cro has been widely used as a standard first-line treatment for locally advanced or metastatic non-small cell lung cancer (Shaw et al. 2020), and used for treating breast cancer in recent studies, Ayoub NM et al. studied the anticancer effects of Cro on breast cancer and the molecular mechanisms associated with these effects. The results showed that multiple HGF/MET pathways are restrained by Cro to achieve the effect of breast cancer treatment (Ayoub et al. 2021).