EnABLing Cathepsin-Driven Melanoma Metastasis

Rakshamani Tripathi; Rina Plattner

doi:10.1080/23723556.2018.1458016

EnABLing Cathepsin-Driven Melanoma Metastasis

Rakshamani Tripathi, Rina Plattner

Pharmacology and Nutritional Sciences

Research output: Contribution to journal › Article › peer-review

Abstract

Metastatic melanoma remains incurable for many due to its aggressive nature. Secreted cathepsins promote metastasis by cleaving matrix and activating pro-invasive proteases. We reported that ABL kinases induce cathepsin secretion and subsequent metastasis by activating ETS1, SP1, and RELA pathways, indicating that ABL inhibitors may serve as novel anti-cathepsin agents.

Original language	English
Article number	e1458016
Journal	Molecular and Cellular Oncology
Volume	5
Issue number	4
DOIs	https://doi.org/10.1080/23723556.2018.1458016
State	Published - Jul 4 2018

Bibliographical note

Funding Information:
This work was supported by NIH grants R01CA116784 and R01CA166499, and by a Markey Cancer Foundation Women Strong Award to R.P. The Research Communications Office of the Markey and Center (P30CA177558) supported this work and contributed to the figure.

Funding Information:
HHS j NIH j National Cancer Institute (NCI), HHS j NIH j National Cancer Institute (NCI). This work was supported by NIH grants R01CA116784 and R01CA166499, and by a Markey Cancer Foundation Women Strong Award to R.P.

Publisher Copyright:
© 2018, © 2018 Taylor & Francis Group, LLC.

Keywords

ABL1
ABL2
Abl
Arg
ETS1
NF-κB
RELA
SP1
cathepsin
cysteine cathepsins

ASJC Scopus subject areas

Molecular Medicine
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1080/23723556.2018.1458016

Cite this

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title = "EnABLing Cathepsin-Driven Melanoma Metastasis",

abstract = "Metastatic melanoma remains incurable for many due to its aggressive nature. Secreted cathepsins promote metastasis by cleaving matrix and activating pro-invasive proteases. We reported that ABL kinases induce cathepsin secretion and subsequent metastasis by activating ETS1, SP1, and RELA pathways, indicating that ABL inhibitors may serve as novel anti-cathepsin agents.",

keywords = "ABL1, ABL2, Abl, Arg, ETS1, NF-κB, RELA, SP1, cathepsin, cysteine cathepsins",

author = "Rakshamani Tripathi and Rina Plattner",

note = "Funding Information: This work was supported by NIH grants R01CA116784 and R01CA166499, and by a Markey Cancer Foundation Women Strong Award to R.P. The Research Communications Office of the Markey and Center (P30CA177558) supported this work and contributed to the figure. Funding Information: HHS j NIH j National Cancer Institute (NCI), HHS j NIH j National Cancer Institute (NCI). This work was supported by NIH grants R01CA116784 and R01CA166499, and by a Markey Cancer Foundation Women Strong Award to R.P. Publisher Copyright: {\textcopyright} 2018, {\textcopyright} 2018 Taylor & Francis Group, LLC.",

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AB - Metastatic melanoma remains incurable for many due to its aggressive nature. Secreted cathepsins promote metastasis by cleaving matrix and activating pro-invasive proteases. We reported that ABL kinases induce cathepsin secretion and subsequent metastasis by activating ETS1, SP1, and RELA pathways, indicating that ABL inhibitors may serve as novel anti-cathepsin agents.

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EnABLing Cathepsin-Driven Melanoma Metastasis

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

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