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Total 75 results found since Jan 2013.

c-Abl phosphorylation of Yin Yang 1's conserved tyrosine 254 in the spacer region modulates its transcriptional activity
In conclusion, we demonstrate the novel role of c-Abl kinase in regulation of YY1's transcriptional activity, linking YY1 regulation with c-Abl tyrosine kinase signaling pathways.
Source: Biochimica et Biophysica Acta (BBA) Molecular Cell Research - May 26, 2018 Category: Molecular Biology Source Type: research

c-Abl phosphorylation of Yin Yang 1's conserved tyrosine 254 in the spacer region modulates its transcriptional activity.
In conclusion, we demonstrate the novel role of c-Abl kinase in regulation of YY1's transcriptional activity, linking YY1 regulation with c-Abl tyrosine kinase signaling pathways. PMID: 29807053 [PubMed - as supplied by publisher]
Source: Biochimica et Biophysica Acta - May 25, 2018 Category: Biochemistry Authors: Daraiseh SI, Kassardjian A, Alexander KE, Rizkallah R, Hurt MM Tags: Biochim Biophys Acta Source Type: research

Inhibition of fibroblast growth factor receptor-signaling sensitizes imatinib-resistant gastrointestinal stromal tumors to low doses of topoisomerase II inhibitors
The acquired resistance of gastrointestinal stromal tumors (GISTs) to the targeted-based therapy remains the driving force to identify the novel approaches that are capable of increasing the sensitivity of GISTs to the current therapeutic regimens. Our present data show that BGJ398, a selective fibroblast growth factor receptor (FGFR) inhibitor, sensitizes imatinib (IM)-resistant GIST cells with receptor tyrosine kinase (RTK) switch (loss of c-KIT/gain of pFGFR2a) to the low doses of topoisomerase II inhibitors – doxorubicin (Dox) and etoposide (Eto). Mechanistically, pretreatment of IM-resistant GIST cells with BGJ398 f...
Source: Anti-Cancer Drugs - May 18, 2018 Category: Cancer & Oncology Tags: Preclinical Reports Source Type: research

CCDC26 knockdown enhances resistance of gastrointestinal stromal tumor cells to imatinib by interacting with c-KIT.
Authors: Cao K, Li M, Miao J, Lu X, Kang X, Zhu H, Du S, Li X, Zhang Q, Guan W, Dong Y, Xia X Abstract Accumulating evidence indicates that long noncoding RNAs (lncRNAs) are involved in diseases such as cancer. However, little is known about the role of lncRNAs in gastrointestinal stromal tumors (GIST). In the present study, we explored the biological function of the lncRNA coiled-coil domain-containing 26 (CCDC26) in imatinib resistance of GIST. We found that human GIST-882 cells with lower CCDC26 expression were less sensitive to imatinib compared with GIST-T1 cells with higher CCDC26 expression. CCDC26 expressio...
Source: American Journal of Translational Research - February 11, 2018 Category: Research Tags: Am J Transl Res Source Type: research

Interleukin 3- receptor targeted exosomes inhibit in vitro and in vivo Chronic Myelogenous Leukemia cell growth
In this study, we engineered HEK293T cells to express the exosomal protein Lamp2b, fused to a fragment of Interleukin 3 (IL3). The IL3 receptor (IL3-R) is overexpressed in CML blasts compared to normal hematopoietic cells and thus is able to act as a receptor target in a cancer drug delivery system. Here we show that IL3L exosomes, loaded with Imatinib or with BCR-ABL siRNA, are able to target CML cells and inhibit in vitro and in vivo cancer cell growth.
Source: Theranostics - September 12, 2017 Category: Molecular Biology Authors: Daniele Bellavia, Stefania Raimondo, Giovanna Calabrese, Stefano Forte, Marta Cristaldi, Agostina Patinella, Lorenzo Memeo, Mauro Manno, Samuele Raccosta, Patrizia Diana, Girolamo Cirrincione, Gianluca Giavaresi, Francesca Monteleone, Simona Fontana, Giac Tags: Research Paper 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

Leukemogenic kinase FIP1L1 ‐PDGFRA and a small ubiquitin‐like modifier E3 ligase, PIAS1, form a positive cross‐talk through their enzymatic activities
In conclusion, our results suggest that sumoylation by PIAS1 is a potential target in the treatment of FIP1L1‐PDGFRA‐positive chronic eosinophilic leukemia. A leukemogenic fusion kinase FIP1L1‐PDGFRA co‐localizes with a SUMO E3 ligase PIAS1 in nucleus. PDGFRA‐C lacking the FIP1L1 portion mainly locates in cytoplasm.
Source: Cancer Science - February 27, 2017 Category: Cancer & Oncology Authors: Makoto Ibata, Junko Iwasaki, Yoichiro Fujioka, Koji Nakagawa, Stephanie Darmanin, Masahiro Onozawa, Daigo Hashimoto, Yusuke Ohba, Shigetsugu Hatakeyama, Takanori Teshima, Takeshi Kondo Tags: Original Article Source Type: research

Opposing roles of KIT and ABL1 in the therapeutic response of gastrointestinal stromal tumor (GIST) cells to imatinib mesylate.
Authors: Rausch JL, Boichuk S, Ali AA, Patil SS, Liu L, Lee DM, Brown MF, Makielski KR, Liu Y, Taguchi T, Kuan SF, Duensing A Abstract Most gastrointestinal stromal tumors (GISTs) are caused by activating mutations of the KIT receptor tyrosine kinase. The small molecule inhibitor imatinib mesylate was initially developed to target the ABL1 kinase, which is constitutively activated through chromosomal translocation in BCR-ABL1-positive chronic myeloid leukemia. Because of cross-reactivity of imatinib against the KIT kinase, the drug is also successfully used for the treatment of GIST. Although inhibition of KIT clea...
Source: Oncotarget - December 16, 2016 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

A leukemogenic kinase, FIP1L1 ‐PDGFRA, and a SUMO E3 ligase, PIAS1, form a positive crosstalk via their enzymatic activities
In conclusion, our results suggest that sumoylation by PIAS1 is a potential target in the treatment of FIP1L1‐PDGFRA‐positive chronic eosinophilic leukemia. This article is protected by copyright. All rights reserved.
Source: Cancer Science - December 12, 2016 Category: Cancer & Oncology Authors: Makoto Ibata, Junko Iwasaki, Yoichiro Fujioka, Koji Nakagawa, Stephanie Darmanin, Masahiro Onozawa, Daigo Hashimoto, Yusuke Ohba, Shigetsugu Hatakeyama, Takanori Teshima, Takeshi Kondo Tags: Original Article Source Type: research

Role of PDGF-D and PDGFR-β in neuroinflammation in experimental ICH mice model.
CONCLUSION: ICH-induced PDGF-D accumulation contributed to post-ICH inflammation via PDGFR activation and enhanced macrophage infiltration. The inhibition of PDGFR had an anti-inflammatory effect. Plasmin is a possible upstream effector of PDGF-D. The targeting of PDGF-D may provide a novel way to decrease brain injury after ICH. PMID: 27302678 [PubMed - as supplied by publisher]
Source: Experimental Neurology - June 10, 2016 Category: Neurology Authors: Yang P, Manaenko A, Xu F, Miao L, Wang G, Hu X, Guo ZN, Hu Q, Hartman RE, Pearce WJ, Obenaus A, Zhang JH, Chen G, Tang J Tags: Exp Neurol 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

Id: 124: abl family kinases mediate lung vascular permeability and inflammation in acute lung injury
Conclusions The Abl family kinases c-Abl and Arg play complementary but distinct roles in mediating vascular permeability and inflammation following LPS challenge. The promoter of Abl1 (c-Abl) contains antioxidant response elements and LPS causes an increase in c-Abl expression. Additionally, LPS increases the mRNA expression of c-Abl, but not Arg. C-Abl contributes to LPS-induced NFB signaling; whereas Arg contributes to inter-endothelial gap formation and adherens junction stability. Inhibition of both of these kinases may be of benefit in patients with ARDS.
Source: Journal of Investigative Medicine - March 21, 2016 Category: Research Authors: Rizzo, A., Letsiou, E., Dudek, S., Sun, X., Garcia, J. Tags: Pulmonary/Critical Care Source Type: research

RalA, a GTPase targeted by miR‑181a, promotes transformation and progression by activating the Ras‑related signaling pathway in chronic myelogenous leukemia.
Authors: Gu C, Feng M, Yin Z, Luo X, Yang J, Li Y, Li T, Wang R, Fei J Abstract BCR/ABL is a well-known activator of multiple signaling pathways. RalA, a Ras downstream signaling molecule and a small GTPase, plays an important role in Bcr-Abl-induced leukemogenesis but the exact mechanism remains elusive. Here, we show that RalA GTPase activity is commonly high in chronic myelogenous leukemia (CML) cell lines and patient samples. Overexpression of RalA results in malignant transformation and progression, and induces resistance to imatinib (IM) in BaF3 and K562 cell lines. RalA reduced survival and led to IM resista...
Source: Oncotarget - March 13, 2016 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

The NESH/Abi-3-based WAVE2 complex is functionally distinct from the Abi-1-based WAVE2 complex
Conclusions: The NESH/Abi-3-based WAVE2 complex is functionally distinct from the Abi-1-based one, and NESH/Abi-3 may be involved in the formation of ventral protrusions under certain conditions.
Source: Cell Communication and Signaling - October 1, 2015 Category: Molecular Biology Authors: Saki SekinoYuriko KashiwagiHitoshi KanazawaKazuki TakadaTakashi BabaSeiichi SatoHiroki InoueMasaki KojimaKatsuko Tani Source Type: research

Revealing genome-wide mRNA and microRNA expression patterns in leukemic cells highlighted “hsa-miR-2278” as a tumor suppressor for regain of chemotherapeutic imatinib response due to targeting STAT5A
This study provides new insights in discovering the mechanism of imatinib resistance due to upregulating the tumor-suppressor hsa-miR-2278 which stands for a functional therapeutic approach, inhibited leukemic cell proliferation, induced apoptosis, and regain of chemotherapeutic drug response in CML therapy.
Source: Tumor Biology - May 8, 2015 Category: Cancer & Oncology Source Type: research