Possible involvement of CCT5, RGS3, and YKT6 genes up-regulated in p53-mutated tumors in resistance to docetaxel in human breast cancers

Ooe, Asako; Kato, Kikuya; Noguchi, Shinzaburo

doi:10.1007/s10549-006-9293-x

Cited by 74 publications

(65 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, Ykt6 can functionally replace Sec22b in ER-toGolgi trafficking (Liu and Barlowe, 2002) and is a more effective suppressor of α-synuclein toxicity than Sec22b (Thayanidhi et al, 2010). In contrast to having a protective role in Parkinson's disease, Ykt6 is found to be upregulated in metastatic tumours (Kluger et al, 2004;Ooe et al, 2007), and moreover, overexpression of Ykt6 in epithelial cell lines accelerates the cell cycle (Thayanidhi et al, 2012). In addition, other recent findings demonstrate that, in neurons, a fraction of the soluble pool of Ykt6 is redirected to large membrane-associated particle aggregates that do not colocalize with any of the known components of the endomembrane system (Hasegawa et al, 2003;Thayanidhi et al, 2012).…”

Section: Sec24mentioning

confidence: 99%

Structure and function of longin SNAREs

Daste

Galli

Tareste

2015

Journal of Cell Science

View full text Add to dashboard Cite

Soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins constitute the core membrane fusion machinery of intracellular transport and intercellular communication.A little more than ten years ago, it was proposed that the long N-terminal domain of a subset of SNAREs, henceforth called the longin domain, could be a crucial regulator with multiple functions in membrane trafficking. Structural, biochemical and cell biology studies have now produced a large set of data that support this hypothesis and indicate a role for the longin domain in regulating the sorting and activity of SNAREs. Here, we review the first decade of structurefunction data on the three prototypical longin SNAREs: Ykt6, VAMP7 and Sec22b. We will, in particular, highlight the conserved molecular mechanisms that allow longin domains to fold back onto the fusioninducing SNARE coiled-coil domain, thereby inhibiting membrane fusion, and describe the interactions of longin SNAREs with proteins that regulate their intracellular sorting. This dual function of the longin domain in regulating both the membrane localization and membrane fusion activity of SNAREs points to its role as a key regulatory module of intracellular trafficking.

show abstract

Section: Sec24mentioning

confidence: 99%

Structure and function of longin SNAREs

Daste

Galli

Tareste

2015

Journal of Cell Science

View full text Add to dashboard Cite

show abstract

“…Ribozymemediated knockdown of RGS3 in aortic smooth muscle cells lead to increased M 3 muscarinic acetylcholine (mAch) receptor-induced MAP kinase activation but no effect on angiotensin II-evoked signaling (Wang et al, 2002a). Elevated levels of RGS3 were found in p53-mutated tumors, and RGS3 siRNA treatment of MCF-7 breast cancer cells resulted in enhanced sensitivity to chemotherapy (docetaxel)-induced apoptosis compared to control (Ooe et al, 2007). Other studies have shown differential levels of RGS3 in multiple cancer screens (Sethakorn and Dulin, 2013) including chronic myeloid leukemia (Luo et al, 2012), pancreatic ductal carcinoma (Zammarchi et al, 2011), soft tissue sarcomas (Takahashi et al, 2006), and gliomas (Tatenhorst et al, 2004).…”

Section: Rgs3mentioning

confidence: 99%

Regulators of G-Protein-Signaling Proteins: Negative Modulators of G-Protein-Coupled Receptor Signaling

Woodard

Jardín

Berna‐Erro

et al. 2015

International Review of Cell and Molecular Biology

View full text Add to dashboard Cite

“…Furthermore cell proliferation signature was present in many tumors and has been associated with poor outcome in a subpopulation of breast cancer patients [42,43]). C16orf61 [DC13], CCT5, and APRT have been previously found to be involved in the phenomenon of multidrug resistance in different carcinomas [44][45][46][47]. CCT5 was found up-regulated in node-positive breast cancer patients with a poor outcome [37].…”

Section: Molecular Biology Of the Markersmentioning

confidence: 99%

Prediction of metastatic relapse in node-positive breast cancer: establishment of a clinicogenomic model after FEC100 adjuvant regimen

Campone¹,

Campion

Roché

et al. 2007

Breast Cancer Res Treat

View full text Add to dashboard Cite

Breast cancer is a very heterogeneous disease, and markers for disease subtypes and therapy response remain poorly defined. For that reason, we employed a retrospective study in node-positive breast cancer to identify molecular signatures of gene expression correlating with metastatic free survival. Patients were primarily included in FEC100 (5-fluorouracil 500 mg/m(2), epirubicin 100 mg/m(2) and cyclophosphamide 500 mg/m(2)) arms of two multicentric prospective adjuvant clinical trials (PACS01 and PEGASE01-FNCLCC cooperative group). Data from nylon microarrays containing 8,032 cDNA unique sequences, representing 5,776 distinct genes, have been used to develop a predictive model for treatment outcome. We obtained the gene expression profiles for 150 of these patients, and used stringent univariate selection techniques based on Cox regression combined with principal component analysis to identify a genomic signature of metastatic relapse after adjuvant FEC100 regimen. Most of the 14 selected genes have a clear role in breast cancer, carcinogenesis or chemotherapy resistance. Six genes have been previously described in other genomic studies (UBE2C, CENPF, C16orf61 [DC13], STMN1, CCT5 and BCL2A1). Furthermore, we showed the interest of combining transcriptomic data with clinical data into a clinicogenomic model for patients subtyping. The described model adds predictive accuracy to that provided by the well-established Nottingham prognostic index or by our genomic signature alone.

show abstract

Possible involvement of CCT5, RGS3, and YKT6 genes up-regulated in p53-mutated tumors in resistance to docetaxel in human breast cancers

Abstract: CCT5, RGS3, and YKT6 mRNA expressions, which are up-regulated in p53-mutated breast tumors, might be implicated in resistance to docetaxel and clinically useful in identifying the subset of breast cancer patients who may or may not benefit from docetaxel treatment.

Cited by 74 publications

References 33 publications

Structure and function of longin SNAREs

Structure and function of longin SNAREs

Regulators of G-Protein-Signaling Proteins: Negative Modulators of G-Protein-Coupled Receptor Signaling

Prediction of metastatic relapse in node-positive breast cancer: establishment of a clinicogenomic model after FEC100 adjuvant regimen

Contact Info

Product

Resources

About