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Characteristics, Events, and Stages in Tumorigenesis
Published in Franklyn De Silva, Jane Alcorn, The Elusive Road Towards Effective Cancer Prevention and Treatment, 2023
Franklyn De Silva, Jane Alcorn
Traditionally, cancer treatment was based on the idea that almost all somatic cells have similar malignant potential [117]. However, tumor tissue is supported by a few dedicated stem cells within the tumor environment [817]. Those cells containing stem cell-like characteristics can give rise to cancers and become a source of cells that give rise to distant metastases [818]. Targeted drugs that cause the regression of primary tumors often fail to eliminate CSCs, placing patients at risk of recurrence, particularly after discontinuation of drug administration [117]. Cancer stem cells can support self-renewal cloning, metastasis, growth, homing, and reproliferation of tumors [819], and give rise to heterogeneous cell populations with high plasticity potential [820, 821], resistance to stressful factors such as low nutrient or oxygen levels, resistance to apoptosis [761, 822], enhanced accumulation of mutations [819], and quiescence [819, 823, 824]. Furthermore, the collective evidence suggests that progenitor cell pools within tumors revert to cancer stem cells through mechanisms such as EMT [819, 825, 826]. EMT is a vital procedure through which nearly all mature tissues sustain their migratory competence in normal embryogenesis, wound healing, and tissue repair [827]. The occurrence of ‘partial EMT' has also been reported in favoring progression and metastasis of cancer [281]. In general, CSCs and undetectable micrometastases continue to be a major challenge in breast and prostate cancer patients and complicate the planning of effective treatment options.
Oncogenesis and Metastasis
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Epithelial-mesenchymal transition (EMT) ‒ loss of connectivity.‘Freely’ allow cancer cells to spread.The inactivation/functional loss of cell adhesion molecule E-cadherin plays a key role in EMT.
Juvenile Polyposis Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Rafael Parra-Medina, Elizabeth E. Montgomery, Paula Quintero-Ronderos, Edgar Garavito
The fact that some tumor samples do not show expression of certain proteins, even though there is evidence of gene structural alteration, suggests epigenetic factors acting as a second hit. They may contribute to the inactivation of genes controlling cell cycle or promoting the activity of tumor progression genes [16]. The relationship of hypoxia with modification of cell behavior is also well described. When a tumor cell divides, the oxygen supply diminishes, thus activating the cell response to hypoxia which depends on the stability of hypoxia-inducible factor 1-alpha (HIF1a). HIF1a is a transcription factor that trans-activates the genes related to erythrocyte production, angiogenesis, and reprogramming of cell metabolism by the increase in aerobic glycolysis [19]. HIF1a also induces expression of genes associated with EMT such as Twist, Snail, Slug, and ZEB1/2, which act during tumor progression, invasion, and metastasis. Therefore, hypoxia modulates the cell behavior, increasing the survival and tumor progression [19]. Finally, the EMT is also related to epigenetic factors that alter the cadherin E expression due to its promoter methylation and the expression of Snail and Slug due to the DNA methylation in their first intronic region. Moreover, miRNAs such as miRNA-200, which is associated with epithelial differentiation, are inhibited by ZEB1 (an EMT activator). Contrarily, p53 increases the expression of miRNA-200. Therefore, a loss of function of this gene is associated with a greater EMT [22]. Any of these factors could be at play in the progression of juvenile polyps to carcinoma.
Epithelial cell dysfunction in chronic rhinosinusitis: the epithelial–mesenchymal transition
Published in Expert Review of Clinical Immunology, 2023
Jing Yuan, Ming Wang, Chengshuo Wang, Luo Zhang
EMT plays an important role in tissue reconstruction, chronic inflammation, tumor growth metastasis, and many fibrotic diseases. Recent studies have demonstrated that EMT is widely present in the nasal mucosa of CRS, especially in CRSwNP, and might be correlated with the degree of severity of disease. EMT occurrence in nasal epithelium not only leads to epithelial cell dysfunction but also plays an important role in nasal tissue remodeling in CRS. Clinically, refractory chronic rhinosinusitis positively correlates with the degree of tissue remodeling. This also implies the significance of EMT in the development of CRS. Since EMT can, in some cases, be reversed. It means mesenchymal cells can turn back into epithelial cells, which makes it possible to treat CRS by acting before permanent nasal mucosal remodeling takes place. Therefore, it is crucial to focus on developing specific medications for EMT. A growing number of studies have recently concentrated on EMT-targeted asthma therapies, but few have looked at how these medications might be employed in CRS.
Transcription factor ETV1-induced lncRNA MAFG-AS1 promotes migration, invasion, and epithelial–mesenchymal transition of pancreatic cancer cells by recruiting IGF2BP2 to stabilize ETV1 expression
Published in Growth Factors, 2023
Hanqin Weng, Weijian Feng, Fengling Li, Dong Huang, Liangyi Lin, Zaiguo Wang
We examined the MAFG-AS1 expression in PC cell lines and found higher MAFG-AS1 in PC cells BxPC-3, SW1990, and PANC-1 and human metastatic PC cell line AsPC-1 than that in HPNE (all p < .05) (Figure 1(A)). AsPC-1 with relatively high expression of MAFG-AS1 was selected for the follow-up study. Subsequently, we studied the effect of MAFG-AS1 on PC cells. RT-qPCR revealed the successful knockdown of MAFG-AS1 in PC cells (Figure 1(B), p < .05). EdU assay showed that knockdown of MAFG-AS1 could significantly inhibit cell proliferation (Figure 1(C), p < .05). Transwell assays exhibited the reduction of migration and invasion of PC cells after the interference of MAFG-AS1 (Figure 1(D,E), all p < .05). EMT is a biological process, which involves cell migration and invasion (Liu et al. 2021). Hence, we further verified whether MAFG-AS1 affects EMT in PC cells. Data from WB showed that the level of epithelial marker (E-cadherin) was elevated in PC cells after knocking down MAFG-AS1, whereas the mesenchymal markers (N-cadherin) and EMT-related protein levels (including Slug and Twist) were reduced (Figure 1(F), p < .05). Briefly, silencing MAFG-AS1 can prevent the proliferation, migration, invasion, and EMT of PC cells.
Molecular Mechanism of Curcumin and Its Analogs as Multifunctional Compounds against Pancreatic Cancer
Published in Nutrition and Cancer, 2022
Qun Huang, Ya Zhang, Yanlin Zheng, Hongjing Yang, Yang Yang, Ya Mo, Liuying Li, Hong Zhang
Abnormal activation of Hedgehog (Hh) signaling plays a significant role in tumorigenesis and metastasis. EMT is involved in the promotion of tumor invasion and metastasis, which are closely related to drug resistance. Moreover, EMT can lead to the reduction or loss of the epithelial marker E-cadherin and induce the production of mesenchymal markers, such as fibronectin protein and vimentin. Sun et al. (59) found that the expression levels of the Hh signaling pathway-related proteins, Shh and GLI1, were significantly reduced, the expression of vimentin was also significantly reduced, while the expression of E-cadherin was increased in PC cells treated with curcumin. These findings indicate that curcumin can reverse EMT by inhibiting the Hh signaling pathway, thereby inhibiting cell proliferation, inducing cell apoptosis, and reducing cell invasion and migration (60).