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Co-targeting of ACK1 and KIT triggers additive anti-proliferative and -migration effects in imatinib-resistant gastrointestinal stromal tumors
Biochim Biophys Acta Mol Basis Dis. 2023 Mar 13:166690. doi: 10.1016/j.bbadis.2023.166690. Online ahead of print.ABSTRACTMost gastrointestinal stromal tumors (GIST) harbor mutated receptor tyrosine kinase (RTK) KIT/PDGFRA, which provides an attractive therapeutic target. However, a majority of GISTs ultimately develop resistance to KIT/PDGFRA inhibitor imatinib, multiple therapeutic targets will be identified as a reasonable strategy in imatinib-resistant GISTs. Biological mechanisms of non-RTK activated CDC42 associated kinase 1 (ACK1) are still unclear, which has been found to be activated in GISTs. In the current report...
Source: Biochimica et Biophysica Acta - March 15, 2023 Category: Biochemistry Authors: Wangzhen He Liangliang Xu Jiongyan Ding Li Song Weili Yang Isabella Klooster Daniel F Pilco-Janeta C ésar Serrano Hongming Fang Guojun Jiang Xiaoyan Wang Jiren Yu Wen-Bin Ou Source Type: research

Hepatoma-Derived Growth Factor and DDX5 Promote Carcinogenesis and Progression of Endometrial Cancer by Activating β-Catenin
Conclusion: Our results provide novel evidence that HDGF interacts with DDX5 and promotes the progression of EC through the induction of β-catenin. Introduction Endometrial cancer (EC) comprises the most common malignancy involving the female genital tract and the fourth most common malignancy in women after breast, lung, and colorectal cancers (1). In 2012, approximately 320,000 new cases of EC were diagnosed worldwide and the incidence is increasing (2). Currently, endometrial carcinogenesis is thought to be a multi-step process involving the coordinated interaction of hormonal regulation, gene mutation, ad...
Source: Frontiers in Oncology - April 10, 2019 Category: Cancer & Oncology 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

MicroRNA-152 inhibits tumor cell growth while inducing apoptosis via the transcriptional repression of cathepsin L in gastrointestinal stromal tumor.
CONCLUSION: The key findings of this study provided evidence suggesting that miR-152 functions by means of binding to CTSL to induce GIST cell apoptosis and inhibit proliferation, migration, and invasion. The anti-tumor role of miR-152 makes it an attractive therapeutic target for GIST. PMID: 29278883 [PubMed - as supplied by publisher]
Source: Cancer Biomarkers : Section A of Disease Markers - December 15, 2017 Category: Cancer & Oncology Authors: Lu HJ, Yan J, Jin PY, Zheng GH, Qin SM, Wu DM, Lu J, Zheng YL Tags: Cancer Biomark 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

GSE80305 Role of COP1 on MAP kinase transcriptional output in gastrointestinal stromal tumor
Contributors : Yu Chen ; Ping ChiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensCOP1 regulates MAP kinase dependent stability Pea3 transcription factors. We determined the role of COP1 in the regulation of MAP kianse transciptional output. We transfected GIST882 cells with siRNA against a scrambled sequence and two sequences against COP1. We treated cells for 8 hours with vehicle or 100 nM PD0325901 in duplicate and isolated RNA for sequencing.
Source: GEO: Gene Expression Omnibus - April 15, 2016 Category: Genetics & Stem Cells Tags: Expression profiling by high throughput sequencing Homo sapiens Source Type: research

Abstract 5484: FGFR2 amplification is predictive of sensitivity to regorafenib in gastric and colorectal cancers
Conclusions Signaling through FGFR2 pathway plays a key role in cellular growth and survival in FGFR2 amplified cancers. Regorafenib effectively abrogates activated FGFR2 signaling in FGFR2 amplified gastric and colorectal cancer cells, and therefore should be considered for integration into treatment in patients with FGFR2 amplified gastric and colorectal cancers.Citation Format: Yongjun Cha, Hwang-Phill Kim, Sae-won Han, Jiyeon Yun, Sang-Hyun Song, Tae-You Kim. FGFR2 amplification is predictive of sensitivity to regorafenib in gastric and colorectal cancers. [abstract]. In: Proceedings of the 106th Annual Meeting of the ...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Cha, Y., Kim, H.-P., Han, S.-w., Yun, J., Song, S.-H., Kim, T.-Y. Tags: Experimental and Molecular Therapeutics Source Type: research

MTOR inhibition enhances NVP-AUY922-induced autophagy-mediated KIT degradation and cytotoxicity in imatinib-resistant gastrointestinal stromal tumors.
Authors: Hsueh YS, Chang HH, Chiang NJ, Yen CC, Li CF, Chen LT Abstract Our previous study demonstrated NVP-AUY922, a HSP90AA1 inhibitor, could enhance mutant KIT degradation in gastrointestinal stroma tumor (GIST) cells through both proteasome- and autophagy-mediated pathways. Herein, we showed rapamycin, a MTOR inhibitor and autophagy inducer, could reduce total and phospho-KIT expression levels and enhance apoptosis in imatinib-resistant GIST cells. The involvement of autophagy in rapamycin-induced KIT downregulation was further confirmed by co-localization of KIT and autophagosome, and partial recovery of KIT e...
Source: Oncotarget - November 12, 2014 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Overexpression of miR-210 is associated with SDH-related pheochromocytomas, paragangliomas, and gastrointestinal stromal tumours
miR-210 is a key regulator of response to hypoxia. Pheochromocytomas (PCs) and paragangliomas (PGLs) with germline SDHx or VHL mutations have pseudohypoxic gene expression signatures. We hypothesised that PC/PGLs containing SDHx or VHL mutations, and succinate dehydrogenase (SDH)-deficient gastrointestinal stromal tumours (GISTs), would overexpress miR-210 relative to non-SDH or -VHL-mutated counterparts. miR-210 was analysed by quantitative PCR in i) 39 PC/PGLs, according to genotype (one SDHA, five SDHB, seven VHL, three NF1, seven RET, 15 sporadic, one unknown) and pathology (18 benign, eight atypical, 11 malignant, two...
Source: Endocrine-Related Cancer - May 6, 2014 Category: Endocrinology Authors: Tsang, V. H. M., Dwight, T., Benn, D. E., Meyer-Rochow, G. Y., Gill, A. J., Sywak, M., Sidhu, S., Veivers, D., Sue, C. M., Robinson, B. G., Clifton-Bligh, R. J., Parker, N. R. Tags: Research Source Type: research