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Showing 1-26 of 26 results for "09-271" within Papers
Matrix metalloproteinase induction of Rac1b, a key effector of lung cancer progression.
Stallings-Mann, ML; Waldmann, J; Zhang, Y; Miller, E; Gauthier, ML; Visscher, DW; Downey et al.
Science Translational Medicine null
Hannah Otterbein et al.
Cancers, 11(8) (2019-08-23)
The small GTPase RAC1B functions as a powerful inhibitor of transforming growth factor (TGF)-β1-induced epithelial-mesenchymal transition, cell motility, and growth arrest in pancreatic epithelial cells. Previous work has shown that RAC1B downregulates the TGF-β type I receptor ALK5, but the
Martin J Baker et al.
Cancers, 12(2) (2020-02-26)
The GTPase Rac1 is a well-established master regulator of cell motility and invasiveness contributing to cancer metastasis. Dysregulation of the Rac1 signaling pathway, resulting in elevated motile and invasive potential, has been reported in multiple cancers. However, there are limited
Catharina Melzer et al.
International journal of molecular sciences, 18(7) (2017-07-21)
Despite improvements in diagnosis and treatment, breast cancer is still the most common cancer type among non-smoking females. TGF-β can inhibit breast cancer development by inducing cell cycle arrest in both, cancer cells and, as part of a senescence program
Rac1b regulates NT3-stimulated Mek-Erk signaling, directing marrow-isolated adult multilineage inducible (MIAMI) cells toward an early neuronal phenotype.
Kevin M Curtis,Lourdes A Gomez,Paul C Schiller
Molecular and Cellular Neurosciences null
David Witte et al.
Scientific reports, 7(1), 17313-17313 (2017-12-13)
Prompted by earlier findings that the Rac1-related isoform Rac1b inhibits transforming growth factor (TGF)-β1-induced canonical Smad signalling, we studied here whether Rac1b also impacts TGF-β1-dependent non-Smad signalling such as the MKK6-p38 and MEK-ERK mitogen-activated protein kinase (MAPK) pathways and epithelial-mesenchymal
Hyunjun Shin et al.
Journal of cellular physiology, 231(8), 1822-1831 (2015-12-15)
The expansion of autologous chondrocytes in vitro is used to generate sufficient populations for cell-based therapies. However, during monolayer culture, chondrocytes lose inherent characteristics and shift to fibroblast-like cells as passage number increase. Here, we investigated passage-dependent changes in cellular
Hendrik Ungefroren et al.
Cancers, 12(12) (2020-12-03)
Autocrine transforming growth factor (TGF)β has been implicated in epithelial-mesenchymal transition (EMT) and invasion of several cancers including pancreatic ductal adenocarcinoma (PDAC) as well as triple-negative breast cancer (TNBC). However, the precise mechanism and the upstream inducers or downstream effectors
Hendrik Ungefroren et al.
Cancers, 14(9) (2022-05-15)
Intratumoral heterogeneity (ITH) is an intrinsic feature of malignant tumors that eventually allows a subfraction of resistant cancer cells to clonally evolve and cause therapy failure or relapse. ITH, cellular plasticity and tumor progression are driven by epithelial-mesenchymal transition (EMT)
Caroline Eiden et al.
Cells, 10(2) (2021-02-12)
Breast cancer (BC) is a heterogenous disease encompassing tumors with different histomorphological phenotypes and transcriptionally defined subtypes. However, the non-mutational/epigenetic alterations that are associated with or causally involved in phenotype diversity or conversion remain to be elucidated. Data from the
Ibuprofen inhibits colitis-induced overexpression of tumor-related Rac1b.
Matos, P; Kotelevets, L; Goncalves, V; Henriques, AF; Henriques, A; Zerbib, P; Moyer et al.
Neoplasia null
Hyun Tae Kang et al.
Aging cell, 16(3), 541-550 (2017-03-21)
Hutchinson-Gilford progeria syndrome (HGPS) constitutes a genetic disease wherein an aging phenotype manifests in childhood. Recent studies indicate that reactive oxygen species (ROS) play important roles in HGPS phenotype progression. Thus, pharmacological reduction in ROS levels has been proposed as
Hendrik Ungefroren et al.
Oncotarget, 5(1), 277-290 (2014-01-01)
Transforming growth factor (TGF)-β1 promotes progression of pancreatic ductal adenocarcinoma (PDAC) by enhancing epithelial-mesenchymal transition, cell migration/invasion, and metastasis, in part by cooperating with the small GTPase Rac1. Prompted by the observation of higher expression of Rac1b, an alternatively spliced
Huizi Wu et al.
International journal of cancer, 143(11), 2962-2972 (2018-08-16)
Recent studies suggest that malignant melanoma heterogeneity includes subpopulations of cells with features of multipotent neural crest (NC) cells. Zebrafish and mouse models have shown that reactivation of neural crest-specific pathways during transformation determines the invasiveness of melanoma cells. In
Hendrik Ungefroren et al.
Cancers, 11(5) (2019-05-22)
The small GTPase Ras-related C3 botulinum toxin substrate 1B (RAC1B) has been shown previously by RNA interference-mediated knockdown (KD) to function as a powerful inhibitor of transforming growth factor (TGF)-β1-induced cell migration and epithelial-mesenchymal transition in epithelial cells, but the
Hiroki Ishii et al.
The Journal of biological chemistry, 289(40), 27386-27399 (2014-08-22)
ESRP1 (epithelial splicing regulatory protein 1) and ESRP2 regulate alternative splicing events associated with epithelial phenotypes of cells, and both are down-regulated during the epithelial-mesenchymal transition. However, little is known about their expression and functions during carcinogenesis. In this study
Christine Mehner et al.
Genes & cancer, 6(11-12), 480-489 (2016-01-26)
Breast, lung, and pancreatic cancers collectively represent one third of all diagnosed tumors and are responsible for almost 40% of overall cancer mortality. Despite improvements in current treatments, efforts to develop more specific therapeutic options are warranted. Here we identify
Christine Mehner et al.
Molecular cancer research : MCR, 12(10), 1430-1439 (2014-05-23)
Pancreatic ductal adenocarcinoma (PDA) arises at the convergence of genetic alterations in KRAS with a fostering microenvironment shaped by immune cell influx and fibrotic changes; identification of the earliest tumorigenic molecular mediators evokes the proverbial chicken and egg problem. Matrix
Hendrik Ungefroren et al.
Cancers, 13(6) (2021-04-04)
Autocrine transforming growth factor β (aTGFβ) has been implicated in the regulation of cell invasion and growth of several malignant cancers such as pancreatic ductal adenocarcinoma (PDAC) or triple-negative breast cancer (TNBC). Recently, we observed that endogenous TGFB1 can inhibit
Larissa Kotelevets et al.
Oncogene, 37(46), 6054-6068 (2018-07-10)
We previously have identified the ectopic expression of Rac1b, an activated and novel splice variant of Rac1, in a subset of human colorectal adenocarcinomas, as well as in inflammatory bowel diseases and in colitis mouse model. Rac1b overexpression has been
Involvement of hnRNP A1 in the matrix metalloprotease-3-dependent regulation of Rac1 pre-mRNA splicing.
Pelisch, F; Khauv, D; Risso, G; Stallings-Mann, M; Blaustein, M; Quadrana, L; Radisky et al.
Journal of Cellular Biochemistry null
Paula M Schmidtlein et al.
Cancers, 13(18) (2021-09-29)
Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive and therapy-resistant cancer types which is largely due to tumor heterogeneity, cancer cell de-differentiation, and early metastatic spread. The major molecular subtypes of PDAC are designated classical/epithelial (E) and quasi-mesenchymal
Joana F S Pereira et al.
Cancers, 14(6) (2022-03-26)
An inflammatory microenvironment is a tumour-promoting condition that provides survival signals to which cancer cells respond with gene expression changes. One example is the alternative splicing variant Rat Sarcoma Viral Oncogene Homolog (Ras)-Related C3 Botulinum Toxin Substrate 1 (RAC1)B, which
Hendrik Ungefroren et al.
Biomedicines, 10(10) (2022-10-28)
Pancreatic ductal adenocarcinoma (PDAC) cells are known for their high invasive/metastatic potential, which is regulated in part by the transforming growth factor β1 (TGFβ1). The involvement of at least two type I receptors, ALK5 and ALK2, that transmit downstream signals
Hendrik Ungefroren et al.
Cancers, 12(6) (2020-06-18)
The small GTPase RAC1B has been shown to act as a powerful inhibitor of the transforming growth factor (TGF)β type I receptor ALK5 and TGFβ1/ALK5-induced epithelial-mesenchymal transition and cell motility. However, the precise mechanism has remained elusive. RNAi-mediated knockdown of
Julia A Newton-Bishop et al.
Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 27(32), 5439-5444 (2009-09-23)
A cohort study was carried out to test the hypothesis that higher vitamin D levels reduce the risk of relapse from melanoma. A pilot retrospective study of 271 patients with melanoma suggested that vitamin D may protect against recurrence of
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