China
Africa
Explore chapters and articles related to this topic
Familial Hyperparathyroidism
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Luigia Cinque, Alfredo Scillitani, Vito Guarnieri
Studies in Drosophila show that Hyrax homolog of human parafibromin is a component of the Wnt/Wg signaling. Parafibromin/Hyrax has been proved to be a positive regulator in the Wnt pathway and is required for nuclear transduction of the WNT/Wg signaling in HEK293 cells. Parafibromin binds directly to the C-terminal region of nuclear β-catenin/Armadillo via its conserved N-terminal domain and recruits other components of the PAF1 complex in order to regulate the transcription of Wnt target genes encoding, for example, the c-Myc oncoprotein and the cell cycle protein cyclin D1 [82,97].
The Non-Hodgkin’s Lymphomas and Plasma Cell Dyscrasias
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
Lynne V. Abruzzo, L. Jeffrey Medeiros
MCLs have clonal rearrangements of the Ig heavy and light chain genes. The TCR genes are usually in the germline configuration. Most cases of MCL contain evidence of the t(11;14)(ql3;q32), either by conventional cytogenetic analysis or by molecular diagnostic techniques. This translocation juxtaposes the immunoglobulin heavy-chain regulatory region on chromosome 14 with the bcl-1 gene (also known as PRAD-1) on chromosome 11, and results in overexpression of the corresponding protein, cyclin D1, a cell cycle protein that is not normally expressed by lymphoid cells. It is believed that the cells are unable to exit the cell cycle.
Retinal stem cell research
Published in A Peyman MD Gholam, A Meffert MD Stephen, D Conway MD FACS Mandi, Chiasson Trisha, Vitreoretinal Surgical Techniques, 2019
Henry Klassen, Michael J Young, Robert Ritch, Julia E Richards, Teresa Borrάs, Leonard A Levin
CNS stem or progenitor cells also express many less specific markers. These include the intermediate filament protein vimentin, the proliferation marker Ki-67, the cell cycle protein cyclin D1, and various forms of the surface adhesion molecule NCAM (neural cell adhesion molecule, CD56), as well as the surface markers CD9 and CD81, both of which are members of the tetraspanin family of transmembrane proteins.5 While it seems increasingly likely that no single unique marker for NSCs will be identified, the use of multiple positive and negative markers in combination may provide a way around this problem. Undoubtedly, a more comprehensive understanding of cellular transcriptional activity will allow investigators to better resolve the ontogenetic status of cells of interest.
Modulating effect of hesperetin on the molecular expression pattern of apoptotic and cell proliferative markers in 7,12-dimethylbenz(a)anthracene-induced oral carcinogenesis
Published in Archives of Physiology and Biochemistry, 2020
Sukumar Babukumar, Veerasamy Vinothkumar, Duraisamy Ramachandhiran
The molecular approach of cancer chemoprevention study utilises apoptotic and cell proliferative proteins and focus on the investigation of the new anticancer agent from a natural source. The tumour suppressor protein p53 is the guardian of the genome and is involved in the regulation of apoptosis, gene amplification and DNA recombination. Mutated-p53 is strongly implicated in several carcinogenesis through the defect in cell-cycle progression and protects cells from apoptosis (Hientz et al.2017). Cyclin-D1 is an important cell-cycle protein that regulates the cell cycle from G1 to S phase through cyclin-dependent kinases. Dysfunction of cell cycle leads to overexpression of cyclin-D1 associated with many cancer types including oral cancer (Duronio and Xiong 2013). Mitochondria by releasing proapoptotic factors contribute to both the caspase-dependent and independent pathways of apoptosis (Alam et al. 2011). In addition initiator (casp-9) and effector (casp-3) caspases are responsible for the stimulation of apoptosis. Decreased caspases expression may prevent the cell from apoptosis that leads to tumorigenesis (Fogarty and Bergmann 2017).
Molecular mechanism of miR-204 regulates proliferation, apoptosis and autophagy of cervical cancer cells by targeting ATF2
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Nan Li, XiaoRong Guo, Lei Liu, Lu Wang, Rongjie Cheng
Activating transcription factor 2 (ATF2) belongs to the alkaline leucine zipper transcription factor family. ATF2 is localized on human chromosome 2q32, plays an inhibitory or promoting role in tumours and participates in cell stress, DNA damage and other processes [21]. Activation of ATF2 is mainly through phosphorylation modification after stress stimulation. Phosphorylated ATF2 binds to specific sequence of promoter region of target gene such as cell cycle molecule, adhesion molecule and apoptosis-related molecule, thereby activating target gene expression. Wu et al. [22] found that ATF2 in renal cell carcinoma can regulate the expression of cell cycle protein B1, cell cycle protein D1, vimentin expression, thereby regulating cell proliferation and metastasis. In addition, previous studies [23] have confirmed that miR-204 can specifically inhibit the expression of ATF2 protein and regulate the proliferation, migration and invasion of human brain keratinocytoma tumour cells. In this study, after transfecting ATF2 siRNA into C33A cells, the expression level of autophagy-related protein LC3I/II was significantly decreased (p < .05), cell viability decreased (p < .05) and apoptosis rate increased (p < .05). When miR-204 mimics and ATF2 siRNA were co-transfected into C33A cells, the inhibitory effect of miR-204 on proliferation and autophagy of C33A cells and its promotion of apoptosis were attenuated.
Deciphering the transcription factor-microRNA-target gene regulatory network associated with graphene oxide cytotoxicity
Published in Nanotoxicology, 2018
Masoumeh Farahani, Mostafa Rezaei–Tavirani, Hakimeh Zali, Afsaneh Arefi Oskouie, Meisam Omidi, Alireza Lashay
Disruption of cell adhesion through the miRNAs appeared to be a response to cytotoxicity that is accompanied by down-regulation of integrins and through the interaction of GO with the focal adhesion pathway. These findings were in agreement with existing research on GO-cell interactions. It has been revealed that GO can be internalized into cytoplasm and nucleus, resulting in decrease of cell adhesion and causing apoptosis (Wang et al. 2011). In particular, Wang et al. reported the cytotoxicity effects of GO on cell adhesive proteins in human fibroblast cells (HDF). They showed that the expression levels of laminin, fibronectin, focal adhesion kinase (FAK; PTK2 protein), and cell cycle protein cyclin D3 in the GO-treated group decrease markedly. Moreover, using the toxicogenomics approach, Zhu et al. demonstrated GO-responsive genes involved in cytoskeletal impairments, focal adhesion pathway, etc. Detailed analysis of their results indicated GO-integrin interactions and confirmed the decline of integrin proteins in GO-exposed J774A.1 (macrophages) and A549 (lung cancer) cells in a dosage-dependent manner. This illustrates that by using this mechanism, GO pretreatment can significantly sensitize A549 lung cancer cells to chemotherapeutic agents (e.g. doxorubicin and cisplatin) (Zhu et al. 2017). Other authors have also shown that GO-derivatives inhibit migration and invasiveness in the metastatic phenotype of cancer cell lines by disruption of the F-actin cytoskeletal assembly and extracellular adhesion (Zhou et al. 2014; Wierzbicki et al. 2017).