Proteomic profiling of human cancer pseudopodia for the identification of anti-metastatic drug candidates

Sunkyu Choi, Aditya Bhagwat, Rasha Al Mismar, Neha Goswami, Hisham Ben Hamidane, Lu Sun, Johannes Graumann

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Abstract

Cancer metastasis causes approximately 90% of all cancer-related death and independent of the advancement of cancer therapy, a majority of late stage patients suffers from metastatic cancer. Metastasis implies cancer cell migration and invasion throughout the body. Migration requires the formation of pseudopodia in the direction of movement, but a detailed understanding of this process and accordingly strategies of prevention remain elusive. Here, we use quantitative proteomic profiling of human cancer pseudopodia to examine this mechanisms essential to metastasis formation, and identify potential candidates for pharmacological interference with the process. We demonstrate that Prohibitins (PHBs) are significantly enriched in the pseudopodia fraction derived from cancer cells, and knockdown of PHBs, as well as their chemical inhibition through Rocaglamide (Roc-A), efficiently reduces cancer cell migration.

Original languageEnglish
Article number5858
JournalScientific Reports
Volume8
Issue number1
DOIs
Publication statusPublished - 1 Dec 2018

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Pseudopodia
Proteomics
Pharmaceutical Preparations
Neoplasms
Neoplasm Metastasis
Cell Movement
Pharmacology

ASJC Scopus subject areas

  • General

Cite this

Proteomic profiling of human cancer pseudopodia for the identification of anti-metastatic drug candidates. / Choi, Sunkyu; Bhagwat, Aditya; Al Mismar, Rasha; Goswami, Neha; Ben Hamidane, Hisham; Sun, Lu; Graumann, Johannes.

In: Scientific Reports, Vol. 8, No. 1, 5858, 01.12.2018.

Research output: Contribution to journalArticle

Choi, Sunkyu ; Bhagwat, Aditya ; Al Mismar, Rasha ; Goswami, Neha ; Ben Hamidane, Hisham ; Sun, Lu ; Graumann, Johannes. / Proteomic profiling of human cancer pseudopodia for the identification of anti-metastatic drug candidates. In: Scientific Reports. 2018 ; Vol. 8, No. 1.
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