Are Parallel Proliferation Pathways Redundant?

Ruth Nussinov, Chung Jung Tsai, Hyunbum Jang

Research output: Contribution to journalReview articlepeer-review

Abstract

Are the receptor tyrosine kinase (RTK) and JAK-STAT-driven proliferation pathways ‘parallel’ or ‘redundant’? And what about those of K-Ras4B versus N-Ras? ‘Parallel’ proliferation pathways accomplish a similar drug resistance outcome. Thus, are they ‘redundant’? In this paper, it is argued that there is a fundamental distinction between ‘parallel’ and ‘redundant’. Cellular proliferation pathways are influenced by the genome sequence, 3D organization and chromatin accessibility, and determined by protein availability prior to cancer emergence. In the opinion presented, if they operate the same downstream protein families, they are redundant; if evolutionary-independent, they are parallel. Thus, RTK and JAK-STAT-driven proliferation pathways are parallel; those of Ras isoforms are redundant. Our Precision Medicine Call to map cancer proliferation pathways is vastly important since it can expedite effective therapeutics.

Original languageEnglish
Pages (from-to)554-563
Number of pages10
JournalTrends in Biochemical Sciences
Volume45
Issue number7
DOIs
StatePublished - Jul 2020

Keywords

  • K-Ras
  • cancer
  • chromatin accessibility
  • drug resistance
  • free energy landscape
  • isoforms
  • precision medicine initiative
  • signaling

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