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Cell Adhesion Migration - Crossref

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Last Updated: 05 July 2022

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Abstract 923: Ibrutinib inhibits malignant cell adhesion and migration and reduces tumor burden in lymph node and bone marrow in a murine model of mantle cell dissemination and progression.

Abstract Abstract: Ibrutnib is a potent and selective Btk inhibitor that covalently modifies Cys481 in Btk and inhibits B cell antigen receptor signaling. Following a dramatic decrease in tumor burden in MCL patients after 1-2 weeks of ibrutinib therapy, we observed a transient rise in MCL cells in peripheral blood suggesting mobilization of malignant cells from tissues to the periphery. Ibrutinib inhibited phosphorylation of Btk, PLC, Erk, and JNK in MCL cell lines and primary MCL cells stimulated by co-culture with stromal cells or anti-IgM. In addition, ibrutinib significantly reduced the manufacture of chemokines CCL3, CCL4, TARC, and CXCL13 in human MCL co-culture or primary MCL cells following BCR activation in MCL cell lines or primary MCL cells. Both MCL cells and patients treated with ibrutinib for either 24 hours or 8 days resulted in over 80% reduction of NF-u03baB, IL-6, CCL3, and CCL4 gene expression in over 80%. In a prevention scheme of MCL lymphadenopathy in SCID mice, Ibrutinib at 3 and 12 mg/kg consistently and dose-dependently reduced tumor burden in the mandibular/cervical lymph nodes, mesenteric lymph nodes, Yesenteric lymph nodes/Peyer Patches, and bone marrow by over 90%. A 90 percent and 68% decrease in tumor cells in the lymph nodes and bone marrow were observed in a therapeutic setting of the same model where tumor injected mice were treated with ibrutinib for six weeks before being given 12 mg/kg of ibrutinib for three weeks.

Source link: https://doi.org/10.1158/1538-7445.am2013-923


Abstract 5603: Minocycline abrogates IL-6 signaling and inhibits migration, invasion and adhesion capacity of ovarian cancer cells.

Minocycline has been described as a drug with pleiotropic abilities, including the reduction of pro-inflammatory cytokine levels. We investigated whether minocycline modulates IL-6, its receptor system, and signaling pathways in ovarian cancer, considering the primary role of IL-6 and its signaling pathways in the development and progression of ovarian cancer. By immunocytochemistry, the expression of IL-6 in control and minocycline-treated ovarian cancer cell lines was determined by immunocytochemistry. In these cell lines, either constitutive and IL-1u03b2 or 4-OH-estradiol stimulated IL-6 expression. Immunocytochemistry and western blot evaluated minocycline's effects on IL-6R expression. The effect of minocycline on the functional status of SKOV-3 cells was determined by adhesion assay and transwell migration and invasion assay, helping to clarify the effect of minocycline against IL-6 bioactivity. The IL-6 levels in plasma and tumor samples excised from these animals were tested by ELISA and western blot in vivo, to determine the effect of minocycline on IL-6 expression in vivo. In vitro, we found that minocycline was potent in suppressing both constitutive and inflaming IL-6 expression. Cell adhesion, migration, and invasion capacity were also found in minocycline-treated cells. It was also discovered that cell adhesion, migration, and invasion capacity were affected by dose-dependent attenuation. Conclusion: These findings showed that minocycline successfully blocks IL-6 signaling in ovarian cancer.

Source link: https://doi.org/10.1158/1538-7445.am2013-5603


Abstract 4339: RGD-conjugated nanoparticles for targeted inhibition of adhesion and migration of integrin αvβ3-overexpressing breast cancer cells.

Methods: The nanoparticle formulation was first optimized with a small amount of RGD target moiety on the nanoparticle surface to increase nanoparticle accumulation in tumors and minimize liver uptake. Solid lipid nanoparticles were synthesized with a fatty acid lipid core and a poly corona and decorated with varying amounts of RGD peptides. The nanoparticle binder of the u03b1v/u03b23 intercellular receptor and in vitro cell uptake in u03b1-u03b21 positive MDA-MB-231 cells was determined by fluorescence microscopy and compared to the results with u03b1b23 negative MCF-7 cells. Standard adhesion and migration assays were used to investigate the effect of RGD-SLNs on cell adhesion and migration by binding to the integrin receptor at u03b1v/u03b23. RGD-SLNs demonstrated specific binding for the u03b1vU3b23 integrin receptors on MDA-MB-231 cells, compared to the negative control group. Clusters of RGD-SLN clusters on the cell membrane and later entered the cells at a slower rate than SLN. In MDA-MB-231 cells, RGD-SLNs had also elevated cellular uptake relative to SLN, although there was no discernable difference between uptake in u03b1vsu03b23 negative MCF-7 cells. Receptor-mediated uptake of RGD-SLNs reduced cell adhesion and migration toward a fibronectin gradient, likely to the receptors being occupied by the RGD-SLN and the slower recycling of the receptors to the cell surface.

Source link: https://doi.org/10.1158/1538-7445.am2013-4339


Abstract 4182: microRNA-29 family as tumor suppressive microRNAs in head and neck squamous cell carcinoma: microRNA-29 a/b/c inhibits cell migration and invasion targeting focal adhesion and ECM pathways.

Abstract BACKGROUND: Squamous cell carcinoma, or head and neck, is the sixth most common malignancy worldwide. The expression of microRNA-29 family in cancer tissues was significantly reduced in cancer cells, according to our microRNA expression signatures of hypopharyngeal squamous cell carcinoma and maxillary sinus SCC. In HNSCC, miR-29a/b/c's aim was to investigate the functional significance of miR-29a/b/c/c/c/c and uncover the novel molecular pathways and responsibility genes regulated by miR-29a/b/c. METHODS: Well-of-function studies were performed to investigate cancer cell proliferation, migration, and invasion by mature miRNAs transfection into HNSCC cell lines, according to METHODS. The expression of miR-29-family target genes was verified in HNSCC clinical samples using a public database of Gene Expression Omnibus. RESULTS: Expression levels of miR-29 family members in HNSCC clinical specimens were dramatically reduced in comparison to nearby non-cancerous tissues. In the HNSCC cell lines, the restoration of each miR-29 family has significantly reduced cancer cell proliferation, migration, and invasion. In clinical HNSCC tumor specimens, three genes — specifically up-regulated relative to normal epithelium — were significantly up-regulated, according to gene expression data. CONCLUSIONS: miR-29 family served as a key promoter of cell migration and invasion in HNSCC by focusing on u201d and u201d signaling pathways. The novel molecular tools to determine whether local tumor recurrence or distant metastasis of HNSCC can be elucidated by the lucidation of tumor suppressive miR-29 family-mediated cancer pathways and putative targets. A tumor suppressive microRNAs in head and neck squamous cell carcinoma inhibit cell proliferation and invasion, according to microRNA-29a/b/c, affecting focal adhesion and ECM pathways.

Source link: https://doi.org/10.1158/1538-7445.am2013-4182


Abstract 4013: S100A4 promotes cell migration and growth through focal adhesion kinase and Src mediated dual signaling pathways in pancreatic cancer cells.

Abstract BACKGROUD: Pancreatic cancer is one of the deadliest forms of cancer. Pancreatic cancers are unusually high in activation and expression of focal adhesion kinase and Src kinase. The findings of clinical trials testing either Src or FAK by inhibitors are mostly unknown. METHODS: In MiaPaca2 and S2VP10 cell lines, the effects of inhibitors on FAK and Src activation, as well as cell migration and growth, were investigated. The effects of FAK or Src mutant expression were determined to see whether FAK and Src depend on each other or independently regulate pancreatic cancer cell phenotypes. Through loss/gain methods, the impact of S100A4 on FAK and Src activation was determined. Immunostining on human pancreatic cancer tissue sections demonstrated the relationship of S100A4 expression with FAK and Src activation. RESULTS: In both MiaPaca2 and S2VP10 cells, FAK and Src kinase inhibitors inhibited transcription in a dose dependent manner. Blocking FAK does not completely prevent Src activation. This is confirmed by the finding that FAK mutant expression largely blocked FAK activation, but not Src activation. In the same way, Src mutant expression did not prevent FAK activation, but it did not block FAK activation. Importantly, increased S100A4 expression has been associated with increased FAK and Src activation in pancreatic cancer. Also, these findings point to the fact that S100A4 promotes the Src-FAK dual signaling pathway, which may contribute to a feed-forward loop that promotes pancreatic tumor formation. Cell migration and growth are promoted by focal adhesion kinase and Src-mediated dual signaling pathways in pancreatic cancer cells.

Source link: https://doi.org/10.1158/1538-7445.am2013-4013


Abstract 1477: Protein Tyrosine Kinase 6 promotes peripheral adhesion complex formation, cell migration, and the epithelial mesenchymal transition in prostate cancer.

Abstract Protein tyrosine kinase 6 is an intracellular tyrosine kinase that is genetically related to Src kinases. Although the majority of total PTK6 is localized within PC3 cells, a human prostate cancer cell line, is membrane-associated, the active pool of PTK6 is membrane-associated. PTK6 activated at the membrane, the establishment of peripheral adhesion complexes, and increased migration of PC3 cells are all triggered by ectopic expression of membrane-targeted PTK6 at the membrane, as well as increased migration of PC3 cells. In vitro and produce more metastases in a xenograft mouse model, while knocking down PTK6 increases epithelial phenotype and inhibits tumor formation in vivo. In normal and metastatic human prostate cancer samples, PTK6 and E-cadherin expressions were reversed, and PTK6 and E-cadherin expressions were detected at the membrane in some high-grade prostate tumors.

Source link: https://doi.org/10.1158/1538-7445.am2013-1477

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions