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Bile Duct Cancer
Published in Dongyou Liu, Tumors and Cancers, 2017
CC is positive for mucin, CEA (cytoplasmic and luminal, not canalicular), CAM 5.2, AE1-AE3, keratin 903 (74%), CK7 (90%–96%) and CK19 (84%); reduced CK903, CK20 (30%–70%, often in nonperipheral tumors), epithelial membrane antigen, amylase, parathyroid hormone (PTH)-related peptide, p53 (10%–94%), proliferating cell nuclear antigen (PCNA), MOC31, and BerEP4, MUC1, MUC4, CD151, p27, COX2, fascin, tenascin, metallothionine, MMP7 may be a favorable prognostic factor; but negative for AFP and HepPar1. Molecularly, CC shows KRAS mutation, downregulation of β-catenin, and aberrant expression and activation of ErbB, hepatocyte growth factor (HGF), and IL6 [5].
Novel therapeutic targets for cancer metastasis
Published in Expert Review of Anticancer Therapy, 2020
Konstantin Stoletov, Perrin H. Beatty, John D. Lewis
Integrin-associated tetraspanin CD151 was determined to be necessary for de-adhesion of cancer cells from the solid tumor, which in turn is an essential first step toward cancer cell intravasation and migration to a secondary lesion site [88]. Blocking this tetraspanin with a CD151 monoclonal antibody resulted in a potent inhibition of cancer cell motility and metastasis [5,69]. Furthermore, this provided evidence that targeting and blocking the functionality of a protein required for multiple metastatic stages was a valid therapeutic anti-metastatic approach. However, it also showed the importance of identifying a therapeutic target that is selective for cancer cells over normal cells. Although CD151 inhibition promoted metastatic cancer cell adhesion to its primary tumor, active CD151 is also necessary for host platelet aggregation and keratinocyte migration in wound healing, which makes CD151 a poor cancer therapeutic agent for use in humans [89]. Since that work, additional genes and regulatory factors in cancer cells have now been found that are essential for cell motility.
Characteristics of circRNA and its approach as diagnostic tool in melanoma
Published in Expert Review of Molecular Diagnostics, 2021
Khatereh Khorsandi, HomaSadat Esfahani, Heidi Abrahamse
CD151 is a member of the transmembrane-4 family with open reading frames contains 253 amino acids. CD151 is largely located in the plasma membrane and found in nearly every cell type [168]. It is determined that CD151 emerged as key players in the organization and regulation of functional membrane protein (such as integrin’s and growth factor receptors). Thereby, it has been implicated in various processes related to physiological and pathological-like ontogenesis [169]. For example, previous studies have shown that high expression levels of CD151 is required to induce the epithelial–mesenchymal transition (EMT) induction and neo-angiogenesis of hepatocellular carcinoma. In fact, the effect of elevated CD151 on the over activation of Integrin α6β1 to PI3K signaling has been studied [170,171]. In melanoma, it has been demonstrated that CD151 amplify cell migration and increase the level of expression of matrix metalloproteinase 9 as the result of stimulating integrin-dependent signal transduction by CD151 affinity interaction [172]. Now, it is confirmed that overexpression of CD151 happens frequently in all types of tumors [173]. In this way, CD151 functions as an oncoprotein and participate in tumor progression, including melanoma. Circ_0020710 is a novel circRNA, which derived from the oncogene CD151. Remarkably, this circRNA was generally overexpressed in melanoma tissues in comparison to healthy tissues, especially in benign nevi tissues. For this reason, circ_0020710 upregulation has a positive correlation with the poor prognosis of melanoma patients. Followed by circ_0020710 increase, CXCL12 is upregulated to promote the progression of melanoma and immune evasion by inducing miR-370-3p sponging. Compared to normal tissues, circ_0020710 is mainly upregulated in all of the melanoma [174].
The involvement of liquid crystals in multichannel implanted neurostimulators, hearing and ENT infections, and cancer
Published in Acta Oto-Laryngologica, 2019
Chouard Claude-Henri, Christiane Binot, Jean-François Sadoc
Tetraspanin-enriched microdomains are regulated by lipids, notably cholesterol, and linked to membrane gangliosides. Like in classic lipid rafts, tetraspanins in sucrose gradients after cell lysis are ‘membrane resistant’; there are, however, differences in behavior compared to classic lipid rafts. Like classic lipid rafts, they are rich in cholesterol and glycosphingolipids, and most tetraspanins associate together due to strong palmitoylation. Electron microscope studies showed that tetraspanin-enriched microdomains showed a mean individual area of 200–400 nm2.Tetraspanins are able to organize membrane microdomains, leading to endocytosis. Association of several microdomains can lead to more extensive platforms. As well as mediating viral attachment and entry, these platforms may be involved in downstream intracellular trafficking of internalized viruses, contributing to virus assembly and exit site organization.Tetraspanins and their microdomains are notably involved in binding between membrane receptors and their extracellular ligands, with receptor oligomerization. These mechanisms can be compared to nanodomain formation on HIV cell entry and Gag protein interaction with PIP2 and PIP3 phosphoinositides, and the PI3K pathway [17]. Again, we would highlight the presence of mesophases in these interactions. Target cell proteins mainly comprise heparan sulfate proteoglycans, integrins, growth factor receptors, actin and tetraspanin CD151. Tetraspanin CD151 binds with actin-linker proteins (ezrin, radixin, moesin), by binding with partner proteins. These interactions need to be explored from the point of view both of the receptor signal and the endocytosis phase, involving membrane phospholipids, which are in an LC state.Plasma membrane tetraspanin-enriched microdomains not only mediate virus entry but are also complexes mediating the various phases of viral infection. It may be that dysfunction of a membrane mesophase or of adjacent tissue or induction by a pathogen can be oncogenic.Lateral coordination of the signaling pathway (i.e. grouping of proteins and lipids, leading to a specific reaction) and enzymatic protein activity modulate CD151 action of cell adhesion, migration, and proliferation. We consider that this lateral coordination leads to onset of a mesogenic state, (which is synonymous with LC state).