MAP17 and the double-edged sword of ROS

Carnero, Amancio

doi:10.1016/j.bbcan.2012.03.004

Cited by 29 publications

(62 citation statements)

References 113 publications

(153 reference statements)

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“…Several of the known MAP17 interactors were clearly represented, such as NHRF1, NHRF2, and PDZK1. We also identified NHE3 (SLC9A3) and other welldescribed interactors, including SLC22A5, SLC15A2, SLC22A4, SLC1A2, ABCC2, and CFTR (32). Furthermore, we found that a majority of the genes were involved in posttranslational modifications related to protein degradation.…”

Section: Map17 Associates With Proteins Involved In Protein Degradationmentioning

confidence: 77%

“…The increased sensitivity to bortezomib observed in MAP17-overexpressing cells depends on the active transport machinery at the membrane Through NHeRF1/3 binding, MAP17 may alter the membrane localization of pumps and transporters, particularly Na þ -coupled transporters (32). Thus, MAP17-overexpressing cells may contain different membrane-associated Na þ -coupled transporters We treated the cells with furosemide in the presence of different concentrations of bortezomib and measured the molecular and physiologic responses to the treatments.…”

Section: Increased Sensitivity Of Map17-overexpressing Cells To Bortementioning

confidence: 99%

“…MAP17 binds several PDZ domain-containing proteins, including PDZK1 (NHRF3) and other NHRF proteins, such as NaPiIIa and NHe3. Together with NHRF3 and NHRF4, overexpression of MAP17 in opossum kidney cells leads to internalization of NaPilla in the trans-Golgi network (30)(31)(32). The physiologic role of MAP17 in proximal tubules is not known; however, MAP17 stimulates specific Na-dependent transport of mannose and glucose in Xenopus oocytes (33) and some human tumor cells (28,34).…”

Section: Introductionmentioning

confidence: 99%

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MAP17 (PDZKIP1) Expression Determines Sensitivity to the Proteasomal Inhibitor Bortezomib by Preventing Cytoprotective Autophagy and NFκB Activation in Breast Cancer

Muñoz-Galván

Gutiérrez

Pérez

et al. 2015

Molecular Cancer Therapeutics

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MAP17 is a small nonglycosylated membrane protein that is overexpressed in a high percentage of carcinomas. High levels of MAP17 enhance the tumorigenic properties of tumor cells by increasing oxidative stress, which is dependent on Na þ -coupled cotransport. Here, we show that MAP17 is associated with proteins involved in protein degradation and that proteasome inhibition induces autophagy. To analyze whether MAP17 could also alter this process, we used the proteasome inhibitor bortezomib (Velcade, PS-341), which is approved for the treatment of multiple myeloma and mantle cell lymphoma, although it has a high rate of resistance emergence and poor efficacy in solid tumors. We provide evidence that bortezomib induces a cytoprotective effect by activating autophagy and NFkB nuclear translocation, responses that are repressed in the presence of high levels of MAP17 both in vitro and in vivo. Indeed, patients with multiple myeloma treated with bortezomib showed higher response rates and a longer time to progression associated with increased levels of MAP17 expression. The MAP17-induced sensitivity to bortezomib is dependent on the oxidative status of the cells and the activity of Na þ -coupled transporters because treatment with antioxidants or the inhibitor furosemide restores the cytoprotective activity induced by bortezomib. Therefore, bortezomib induces a prosurvival response through cytoprotective autophagy and NFkB nuclear translocation, which is repressed by high levels of MAP17. We propose that the levels of MAP17 could be used as a prognostic marker to predict the response to bortezomib in hematologic malignancies and in other tissues that are not commonly responsive to the drug.

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Section: Map17 Associates With Proteins Involved In Protein Degradationmentioning

confidence: 77%

Section: Increased Sensitivity Of Map17-overexpressing Cells To Bortementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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MAP17 (PDZKIP1) Expression Determines Sensitivity to the Proteasomal Inhibitor Bortezomib by Preventing Cytoprotective Autophagy and NFκB Activation in Breast Cancer

Muñoz-Galván

Gutiérrez

Pérez

et al. 2015

Molecular Cancer Therapeutics

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“…It was reported that MAP17 harbored the ability of tumorigenesis by increasing endogenous reactive oxygen species (ROS) (22). The increased ROS activates AKT and significantly decreases c-myc-induced apoptosis through SGLT1 activation (23), and the suppression of SGLT1 inhibits MAP17-induced ROS increase and tumor cell proliferation (24).…”

Section: Map17 Expression Was Upregulated and Associated With Tki Resmentioning

confidence: 99%

EGFR-TKI resistance and MAP17 are associated with cancer stem cell like properties

Shao

Zhong

et al. 2018

Oncol Lett

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Abstract.Patients with non-small-cell lung cancer (NSCLC) with sensitive epidermal growth factor receptor (EGFR) mutations generally react well to tyrosine kinase inhibitors (TKIs). However acquired resistance eventually occurs. Several mechanisms contribute to the resistance including T790M mutation, c-Met amplification and PIK3CA mutation. In recent years, cancer stem cells (CSCs) have been suggested to be involved in TKI resistance. MAP17 is aberrantly overexpressed in a number of malignancies. However, the expression pattern and function of MAP17 in CSCs are still unclear. The aim the present study was to illustrate the effect of CSC-like cells on the resistance to TKIs in EGFR mutant NSCLC cells and explore the possible role of MAP17 in CSCs. The EGFR mutant cell line PC9 was cultured under serum-deprived undifferentiated conditions. The CSC properties including expression of stem cell markers CD133, CD44, Oct-4 and ABCG2, ability of self-renewal, invasion, proliferation and tumorigenesis were examined. The expression of MAP17 was compared in sphere and parent cells. Sphere cells displayed stem cells phenotypes and were resistant to erlotinib. Sphere cells expressed higher levels of MAP17, and MAP17 was associated with self-renewal and TKI resistance. The function of MAP17 demonstrated to be partially dependent on Na-dependent glucose transporter 1. Collectively these findings suggest that MAP17 serves a role in TKI resistance through regulation of CSCs in lung cancer.

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“…In contrast, excessive ROS can be important mediators of damage to cell structures, including lipids, proteins and nucleic acids. Furthermore, these ROS-induced damages may lead to the effects of aging and a variety of diseases such as chronic inflammatory disease, cardiovascular disease and cancer [2,3].…”

Section: Introductionmentioning

confidence: 99%

Ingestion of Tabebuia avellanedae (Taheebo) Inhibits Production of Reactive Oxygen Species from Human Peripheral Blood Neutrophils

Ohno¹,

Ohno²,

Suzuki³

et al. 2015

IJFS

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MAP17 and the double-edged sword of ROS

Cited by 29 publications

References 113 publications

MAP17 (PDZKIP1) Expression Determines Sensitivity to the Proteasomal Inhibitor Bortezomib by Preventing Cytoprotective Autophagy and NFκB Activation in Breast Cancer

MAP17 (PDZKIP1) Expression Determines Sensitivity to the Proteasomal Inhibitor Bortezomib by Preventing Cytoprotective Autophagy and NFκB Activation in Breast Cancer

EGFR-TKI resistance and MAP17 are associated with cancer stem cell like properties

Ingestion of Tabebuia avellanedae (Taheebo) Inhibits Production of Reactive Oxygen Species from Human Peripheral Blood Neutrophils

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