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Role of dendritic cells in integrating immune responses to luminal antigens
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Brian L. Kelsall, Maria Rescigno
Pre-cDCs differentiate in the bone marrow in response to Flt3L and mature into two primary cDC populations, cDC1 and cDC2 cells, in tissues and lymphoid organs under the influence of the hematopoietic cytokines Flt3L, GM-CSF, and unique transcription factors. cDC1 cells are CD103+CD8+CD11b− (SIRPα−, XCR1+) and are dependent on the transcription factors BATF3, IRF8, and Id2, whereas cDC2 cells are CD103+CD11b+ (SIRPα+, XCR1−) and dependent on IRF4, KLF4, and Notch 2. These populations also have been identified in other species, including humans, the definitions of which depend on the expression of CD103, XCR1, and SIRPα, which have emerged as more reliable markers than CD11b and CD8 across species. In the mouse intestine, an additional population of pre-cDC-derived CD103−CD11b+ XCR1− DCs uniquely shares developmental dependence on the transcription factor Zeb2 with monocyte-derived cells and expresses intermediate levels of CX3CR1 that is present at high levels on macrophages. This population is considered a unique DC lineage, as it is derived from pre-cDCs and dependent on FLT3L for its differentiation.
Blastic Plasmacytoid Dendritic Cell Neoplasms (BPDCN)
Published in Dongyou Liu, Tumors and Cancers, 2017
Molecularly, BPDCN is linked to multiple karyotypic abnormalities (e.g., chromosomes 5q [72%], 12p [64%], 13q [64%], 6q [50%], 15q [43%], and monosomy 9 [28%]) and genetic mutations involving 9p21.3 (CDKN2A/CDKN2B, 50%), 13q13.1-q14.3 (RB1, 43%), 12p13.2-p13.1 (CDKN1B, 64%), 13q11-q12 (LATS2), TET2 (36%–80%), ASXL1 (32%), NPM1 (20%), NRAS (20%), IKZF1 (20%), IKZF1-3 (20%), ZEB2 (16%), TP53 (14%), HOXB9 (4%), and UBE2G2 (4%) [4,5].
Structure and function of the mesothelial cell
Published in Wim P. Ceelen, Edward A. Levine, Intraperitoneal Cancer Therapy, 2015
Steven E. Mutsaers, Cecilia M. Prêle, Sarah E. Herrick
Epithelial to mesenchymal transition (EMT) is a basic biological process that is involved in embryogenesis, tissue repair, and numerous pathologies, including organ fibrosis, malignant transformation, and cancer progression. The processes that occur during pathological EMT are thought to be comparable to physiological EMT as they are controlled by similar signaling pathway regulators and effector molecules. When exposed to certain growth factors and/or injurious agents, epithelial cells undergo a complex morphological transition and acquire a mesenchymal phenotype. This complex process is primarily controlled by three main families of transcription factors: snail family zinc finger (SNAI1, SNAI2), basic helix-loop-helix (TWIST1), and zinc finger E-box-binding homeobox (ZEB1, ZEB2) [10]. Epithelial cells initially lose cell–cell junctions, attachment to basement membrane, and apical–basal cell polarity. Of importance, loss of cell surface junctional protein E-cadherin is a prerequisite for EMT. With subsequent migration and invasion through the basement membrane and a change in cytoskeletal components, a full change to a mesenchymal phenotype occurs. Expression of a multitude of mesenchymal markers, including α-SMA, EDA-fibronectin, vimentin, and fibroblast-specific protein-1, is proposed to be an indicator that EMT has occurred [11]. The profibrotic mediator, transforming growth factor-β1 (TGF-β1), represents a major inducer of EMT, whereas bone morphogenic protein 7 has been identified as a repressor in certain tissues [12]. MicroRNAs (miRs) have recently emerged as important regulators of EMT as they are able to target multiple signaling pathways [13].
MiR-454-3p promotes apoptosis and autophagy of AML cells by targeting ZEB2 and regulating AKT/mTOR pathway
Published in Hematology, 2023
Xiao Wang, Liang Zhong, Wenran Dan, Xuan Chu, Xu Luo, Chen Liu, Peng Wan, Yang Lu, Zhenyan Liu, Zhonghui Zhang, Beizhong Liu
Apoptosis and autophagy are two types of programd cell death triggered by common upstream signals with complex functional interrelationships. Autophagy has been shown to suppress apoptosis and represents a stress adaptation to avoid cell death under certain conditions [23]. Intrestingly, under different conditions, autophagy may stimulate apoptosis [24,25]. In our study, ZEB2 was found to participate in the suppression of apoptosis and autophagy. Simultaneously, we questioned if ZEB2 knockdown could trigger apoptosis in AML cells via enhancing autophagy in our research. Exposure of ZEB2-knockdown THP-1 cells to 3-MA produced decreased levels of apoptosis-associated proteins (Figure 5e). Thus, autophagy appears to induce apoptosis in the system used during the current study. ZEB2 knockdown promoted apoptosis by enhancing autophagic activity in the AML cell-line.
The expression of BMP, integrin, ZEB2 in ovarian high-grade serous carcinoma in relation with lymph node metastasis
Published in Growth Factors, 2022
Elham Bahador Zırh, Elif Taşar Kapaklı, Anıl Dolgun, Alp Usubütün, Naciye Dilara Zeybek
Smad-interacting protein-1 (Sip1, also named as ZEB2) was one of the first identified SIPs, and it was originally identified as a transcription factor which play vital roles in the TGF-β signaling cascade (Verschueren et al. 1999). ZEB2 plays an important role during tumorigenesis. Previous studies have documented that ZEB2 acts as a transcriptional repressor of E-cadherin and plays a role in epithelial-mesenchymal transition (EMT) in breast and liver cancers (Conidi et al. 2013). Knockdown of ZEB2 impaired migration, invasion and anchorage-independent cell growth and indicated a pivotal role of ZEB2 in the progression of ovarian carcinogenesis (Prislei et al. 2015). Besides transcription factors, integrins play a role in metastasis through various cellular activities such as cell migration-invasion, cell proliferation, cell survival-apoptosis, cell to ECM binding and cell cycle (Ganguly et al. 2013). Metastatic cells that undergo EMT adhere to the tissue by integrins during and after migration. Integrins increase in metastasis of many cancer types, including OCs (Berrier and Yamada 2007; Ganguly et al. 2013). αvβ6, β1, α5β1, β4 integrins play a role in metastasis and invasion in OC (Ganguly et al. 2012). The increase in β1-integrin in epithelial OCs associated with increased metastasis of cancer cells. Inhibition of β1 integrin reduced cell motility in the same study (Chen et al. 2016).
Interaction between CASP8AP2 and ZEB2-CtBP2 Regulates the Expression of LEF1
Published in Pediatric Hematology and Oncology, 2022
Chan-Juan Wang, Ming-Zhu Jia, Li-Ping Deng, Wei-Jing Li, Qing Zhang, Tong-Jia Zhang, Shu-Yan Li, Lei Cui, Zhi-Gang Li
ZEB is an important intranuclear transcription factor. There are two highly homologous members in vertebrates, ZEB1 and ZEB2, both of which are structurally similar and can interact with CtBP to exert transcriptional repression.7 Research has shown that ZEB2 is associated with early T cell differentiation and development as well as T-ALL,10 and the positive rate of ZEB2 expression in children with ALL is close to 100%.11 Recently, it has been reported that CASP8AP2 interacts with ZEB1 to maintain its stability by inhibiting ubiquitination of ZEB1, thereby supporting transformational growth factor-β (TGF-β)-induced epithelial-to-mesenchymal transition (EMT).12