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Total 75 results found since Jan 2013.

Attenuation of fibrosis with selective inhibition of c-Abl by siRNA in systemic sclerosis dermal fibroblasts
In conclusion, specific c-Abl gene silencing using siRNA effectively reduced fibrosis-related gene expression. Inhibition of c-Abl by siRNA may be a potential therapeutic approach for fibrotic diseases such as systemic sclerosis.
Source: Archives of Dermatological Research - December 20, 2014 Category: Dermatology Source Type: research

Melanoma Cancer Immunotherapy Using PD-L1 siRNA and Imatinib Promotes Cancer-Immunity Cycle
ConclusionOverall, results revealed that the tumors treated with siPDIN restored the immunity of CTLs by potentially inhibiting the immune checkpoint interactions, suppressed the mTOR signaling pathway and exhibited an enhanced anticancer efficacy in melanoma.
Source: Pharmaceutical Research - May 30, 2020 Category: Drugs & Pharmacology Source Type: research

A combination of STI571 and BCR-ABL1 siRNA with overexpressed p15INK4B induced enhanced proliferation inhibition and apoptosis in chronic myeloid leukemia.
In conclusion, our study may provide new insights into the role of p15INK4B in CML and a potential therapeutic target for overcoming tyrosine kinase inhibitor resistance in CML. PMID: 25387678 [PubMed - in process]
Source: Braz J Med Biol Res - November 16, 2014 Category: Research Authors: Xia DY, Liu L, Hao MW, Liu Q, Chen RA, Liang YM Tags: Braz J Med Biol Res Source Type: research

Expression of inducible NOS is indispensable for the antiproliferative and proapoptotic effect of imatinib in BCR-ABL positive cells.
Abstract Chronic myeloid leukemia (CML) is characterized by constitutive BCR-ABL kinase activity, an aggressive proliferation of immature cells, and reduced differentiation. Targeting tyrosine kinase activity of BCR-ABL with imatinib is an effective therapy for the newly diagnosed CML patients; however, 20%-30% of the patients initially treated with imatinib eventually experience treatment failure. Therefore, early identification of these patients is of high clinical relevance. In the present study, we by undertaking a direct comparison of inducible NOS (iNOS) status in neutrophils from healthy volunteers, newly d...
Source: Journal of Leukocyte Biology - February 2, 2021 Category: Hematology Authors: Singh AK, Awasthi D, Dubey M, Nagarkoti S, Chandra T, Barthwal MK, Tripathi AK, Dikshit M Tags: J Leukoc Biol Source Type: research

Sphingomyelin synthase 1 activity is regulated by the BCR-ABL oncogene Research Articles
Sphingomyelin synthase (SMS) produces sphingomyelin while consuming ceramide (a negative regulator of cell proliferation) and forming diacylglycerol (DAG) (a mitogenic factor). Therefore, enhanced SMS activity could favor cell proliferation. To examine if dysregulated SMS contributes to leukemogenesis, we measured SMS activity in several leukemic cell lines and found that it is highly elevated in K562 chronic myelogenous leukemia (CML) cells. The increased SMS in K562 cells was caused by the presence of Bcr-abl, a hallmark of CML; stable expression of Bcr-abl elevated SMS activity in HL-60 cells while inhibition of the tyr...
Source: The Journal of Lipid Research - February 12, 2013 Category: Lipidology Authors: Burns, T. A., Subathra, M., Signorelli, P., Choi, Y., Yang, X., Wang, Y., Villani, M., Bhalla, K., Zhou, D., Luberto, C. Tags: Research Articles Source Type: research

Proliferation inhibition and apoptosis induction of imatinib-resistant chronic myeloid leukemia cells via PPP2R5C down-regulation
In conclusion, the suppression of PPP2R5C by RNA interference could inhibit proliferation and effectively induce apoptosis in CML cells that were either imatinib sensitive or resistant. Down-regulating PPP2R5C gene expression might be considered as a new therapeutic target strategy for CML, particularly for imatinib-resistant CML.
Source: Journal of Hematology and Oncology - September 3, 2013 Category: Hematology Authors: Qi ShenSichu LiuYu ChenLijian YangShaohua ChenXiuli WuBo LiYuhong LuKanger ZhuYangqiu Li Source Type: research

Inhibition of STAT3-interacting protein 1 (STATIP1) promotes STAT3 transcriptional up-regulation and imatinib mesylate resistance in the chronic myeloid leukemia
Conclusions: Our data suggest that STATIP1 may be a negative regulator of STAT3 and demonstrate its involvement in IM therapy resistance in CML.
Source: BMC Cancer - November 23, 2014 Category: Cancer & Oncology Authors: André MencalhaStephany CorrêaDaniela SallesBárbara Du RocherMarcelo SantiagoEliana Abdelhay Source Type: research

Id: 109: parkin mediates endothelial pro-inflammatory responses in acute lung injury
Conclusion These results suggest that endothelial parkin mediates EC activation and neutrophil adhesion/migration after LPS, and therefore it may represent a new potential therapeutic target in ALI/ARDS.
Source: Journal of Investigative Medicine - March 21, 2016 Category: Research Authors: Letsiou, E., Wang, H., Belvitch, P., Dudek, S., Sammani, S. Tags: Pulmonary/Critical Care Source Type: research

Bcl6 gene-silencing facilitates PMA-induced megakaryocyte differentiation in K562 cells.
Abstract Targeted therapy via imatinib appears to be a promising approach for chronic myeloid leukemia (CML) therapy. However, refractory and resistance to imatinib therapy has encouraged many investigators to get involved in development of new therapeutic agents such as Phorbol 12-myrestrat 13-acetate (PMA) for patients with CML. In that line, we attempted to investigate the chemosensitizing effect of PMA on the imatinib-resistant cells. Based on our western blot analyses, resistant K562 cells (K562R) showed high levels of FoxO3a and Bcl6 expressions which were not modulated by imatinib treatment. However, upon P...
Source: Journal of Cell Communication and Signaling - June 6, 2017 Category: Molecular Biology Authors: Eskandari S, Yazdanparast R Tags: J Cell Commun Signal Source Type: research

Aurora Kinase a/MDM2-Mediated SETD2 Loss of Function in Chronic Myeloid Leukemia Patients in Blast Crisis Induces Genetic Instability and Can be Therapeutically Targeted
In conclusion, phosphorylation by Aurora Kinase A and ubiquitination by MDM2 contribute to SETD2 non-genomic loss of function in advanced-phase CML. Loss of SETD2/H3K36me3 is associated with increased DNA damage and impaired HR repair. Restoring physiological H3K36me3 levels may help improve the outcome of this critical subset of pts.Acknowledgments: study supported by AIRC (project code 16996) and AIL (Associazione Italiana contro le Leucemia, Linfomi e Mieloma).Figure 1.DisclosuresCastagnetti: Incyte: Consultancy, Honoraria; Pfizer: Consultancy, Honoraria; Bristol Meyers Squibb: Consultancy, Honoraria; Novartis: Consulta...
Source: Blood - November 21, 2018 Category: Hematology Authors: Mancini, M., De Santis, S., Monaldi, C., Bavaro, L., Martelli, M., Castagnetti, F., Gugliotta, G., Rosti, G., Fontana, M. C., Dan, E., Sinigaglia, B., Iurlo, A., Orofino, N., Abruzzese, E., Salvucci, M., Pregno, P., Gozzini, A., Crugnola, M., Albano, F., Tags: 631. Chronic Myeloid Leukemia: Biology and Pathophysiology, excluding Therapy: Poster I Source Type: research

Simvastatin preparations promote PDGF-BB secretion to repair LPS-induced endothelial injury through the PDGFR β/PI3K/Akt/IQGAP1 signalling pathway.
Simvastatin preparations promote PDGF-BB secretion to repair LPS-induced endothelial injury through the PDGFRβ/PI3K/Akt/IQGAP1 signalling pathway. J Cell Mol Med. 2019 Oct 01;: Authors: Zheng X, Zhang W, Wang Z Abstract Endothelial barrier dysfunction is a critical pathophysiological process of sepsis. Impaired endothelial cell migration is one of the main reasons for endothelial dysfunction. Statins may have a protective effect on endothelial barrier function. However, the effect and mechanism of statins on lipopolysaccharide (LPS)-induced endothelial barrier dysfunction remain unclear. Simvastatin ...
Source: J Cell Mol Med - September 30, 2019 Category: Molecular Biology Authors: Zheng X, Zhang W, Wang Z Tags: J Cell Mol Med Source Type: research

Induction of autophagy by imatinib sequesters Bcr‐Abl in autophagosomes and down‐regulates Bcr‐Abl protein
In this study, we show that following Imatinib treatment, Bcr‐Abl is sequestered into vesicular structures that co‐localize with the autophagy marker LC3 or GABARAP. This association is inhibited by siRNA mediated knockdown of autophagy regulators (Beclin 1/ATG7). Pharmacological inhibition of autophagy also reduced Bcr‐Abl/LC3 co‐localization in both K562 and CML patient cells. Bcr‐Abl protein expression was reduced with Imatinib treatment. Inhibition of both autophagy and proteasome activity in Imatinib treated cells was required to restore Bcr‐Abl protein levels to those of untreated cells. This ability to d...
Source: American Journal of Hematology - February 26, 2013 Category: Hematology Authors: Baukje M. Elzinga, Michelle J. Nyhan, Lisa C. Crowley, Tracey R. O'Donovan, Mary R. Cahill, Sharon L. McKenna Tags: Research Article Source Type: research

Imatinib mesylate inhibits cell growth of malignant peripheral nerve sheath tumors in vitro and in vivo through suppression of PDGFR-beta
Conclusions: The results suggest that imatinib mesylate may be useful in the treatment of MPNST patients and in vitro studies may help select cells that are sensitive to imatinib mesylate in vivo.
Source: BMC Cancer - May 4, 2013 Category: Cancer & Oncology Authors: Jun OhishiMikiko AokiKazuki NabeshimaJunji SuzumiyaTamotsu TakeuchiAkira OgoseMichiyuki HakozakiYuichi YamashitaHiroshi Iwasaki Source Type: research

AMPK Inhibits Oxidative Stress-induced Caveolin-1 Phosphorylation Cell Biology
Caveolin-1 is the primary structural component of endothelial caveolae that is essential for transcellular trafficking of albumin and is also a critical scaffolding protein that regulates the activity of signaling molecules in caveolae. Phosphorylation of caveolin-1 plays a fundamental role in the mechanism of oxidant-induced vascular hyper permeability. However, the regulatory mechanism of caveolin-1 phosphorylation remains unclear. Here we identify a previously unexpected role for AMPK in inhibition of caveolin-1 phosphorylation under oxidative stress. A pharmacological activator of AMPK, 5-amino-4-imidazole carboxamide ...
Source: Journal of Biological Chemistry - July 12, 2013 Category: Chemistry Authors: Takeuchi, K., Morizane, Y., Kamami-Levy, C., Suzuki, J., Kayama, M., Cai, W., Miller, J. W., Vavvas, D. G. Tags: Signal Transduction Source Type: research

The role of TC-PTP (PTPN2) in modulating sensitivity to imatinib and interferon-α in CML cell line, KT-1 cells
Abstract: T-cell protein tyrosine phosphatase (TC-PTP, also known as PTPN2) is a negative regulator of the JAK/STAT pathway. STAT5 is activated by BCR-ABL kinase and STAT1 is an important transcription factor for interferon (IFN)-α-induced signaling in chronic myeloid leukemia (CML). We used siRNA to delete TC-PTP in the CML cell line, KT-1, and examined changes in the sensitivity to imatinib and IFN-α. Suppression of TC-PTP induced activation of STAT5, leading to imatinib resistance, while prolonged phosphorylation of STAT1 was induced by IFN-α, triggering cell death in KT-1 cells. These findings suggest that TC-PTP mo...
Source: Leukemia Research - June 6, 2013 Category: Hematology Authors: Yuriko Nishiyama-Fujita, Takatsune Shimizu, Morihiko Sagawa, Hideo Uchida, Masahiro Kizaki Tags: Laboratory Studies Source Type: research