Abstract

Targeting ncRNAs in the 3q26.2 amplicon.

Highlights

  • Studies from our laboratory and others have revealed that copy number aberrations (CNA) of 3q26.2 lead to aberrant expression of a set of potential oncogenes including PIK3CA, PIK3CB, PKCt, SNON, MECOM as well as TERC in ovarian and other cancers [5], suggesting that multiple components in the amplicon contribute to tumor initiation and progression either alone or in cooperation

  • TP53INP1 binds to homeodomain-interacting protein kinase 2 (HIPK2), which phosphorylates p53 on Ser-46 [6]

  • Loss of TP53INP1 has been associated with coordinate decreases in several tumor suppressors including P53AIP1, caspase-3, and p21, and impaired cell cycle regulation and apoptosis [8]

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Summary

Introduction

Studies from our laboratory and others have revealed that copy number aberrations (CNA) of 3q26.2 lead to aberrant expression of a set of potential oncogenes including PIK3CA, PIK3CB, PKCt, SNON, MECOM as well as TERC in ovarian and other cancers [5], suggesting that multiple components in the amplicon contribute to tumor initiation and progression either alone or in cooperation. Loss of TP53INP1 has been associated with coordinate decreases in several tumor suppressors including P53AIP1, caspase-3, and p21, and impaired cell cycle regulation and apoptosis [8]. The decrease in TP53INP1 expression during preneoplastic development as well as in many types of cancers may interrupt the function of p53 [4, 9].

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