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Rnf126 as a biomarker of a poor prognosis in invasive breast cancer and chek1 inhibitor efficacy in breast cancer cells

  • Xiaosong Yang
    ,
  • You Pan
    ,
  • Zhaojun Qiu
    ,
  • Zhanwen Du
    ,
  • Yao Zhang
    ,
  • Pengyan Fa
*Corresponding author for this work
  • Case Western Reserve University
    ,
  • Sun Yat-Sen University
    ,
  • Cleveland State University
    ,
  • Washington University St. Louis
    ,
  • CAS - Kunming Institute of Zoology
    ,
  • University of Maryland, Baltimore
Scholary Output:
Contribution to journal
Article
Peer-review

Open access

Sustainable Development Goals

  • SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well

Abstract

Purpose: (i) To investigate the expression of the E3 ligase, RNF126, in human invasive breast cancer and its links with breast cancer outcomes; and (ii) to test the hypothesis that RNF126 determines the efficacy of inhibitors targeting the cell-cycle checkpoint kinase, CHEK1. Experimental Design: A retrospective analysis by immunohis-tochemistry (IHC) compared RNF126 staining in 110 invasive breast cancer and 78 paired adjacent normal tissues with clinicopathologic data. Whether RNF126 controls CHEK1 expression was determined by chromatin immunoprecipitation and a CHEK1 promoter driven luciferase reporter. Staining for these two proteins by IHC using tissue microarrays was also conducted. Cell killing/replication stress induced by CHEK1 inhibition was evaluated in cells, with or without RNF126 knockdown, by MTT/ colony formation, replication stress biomarker immunostaining and DNA fiber assays. Results: RNF126 protein expression was elevated in breast cancer tissue samples. RNF126 was associated with a poor clinical outcome after multivariate analysis and was an independent predictor. RNF126 promotes CHEK1 transcript expression. Critically, a strong correlation between RNF126 and CHEK1 proteins was identified in breast cancer tissue and cell lines. The inhibition of CHEK1 induced a greater cell killing and a higher level of replication stress in breast cancer cells expressing RNF126 compared to RNF126 depleted cells. Conclusions: RNF126 protein is highly expressed in invasive breast cancer tissue. The high expression of RNF126 is an independent predictor of a poor prognosis in invasive breast cancer and is considered a potential biomarker of a cancer's responsiveness to CHEK1 inhibitors. CHEK1 inhibition targets breast cancer cells expressing higher levels of RNF126 by enhancing replication stress.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 1629-1643 (15 pages)

Journal (Volume, Issue Number)

Clinical Cancer Research (Volume 24, Issue 7)

Publication milestones

  • Published - 04/01/2018

Publication status

Published - 04/01/2018

ISSN

1078-0432

Publication IDs

  • Scopus: 85047878746
  • PubMed: 29326282

Publication metrics

Metrics

Fractional count
1
Fractional count
0.06
Fractional count
15
Fractional count
0.94
Fractional count
1
Fractional count
1
Scopus
citations
SciVal
citations
13
SciVal
FWCI
1.12
SciVal
Author count
16
SciVal
Paper percentile
86

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Citation count
37
Captures
32

Funding Details

Science Foundation of China grant (31571452 and 31271503) and Guangdong Provincial Natural Science Foundation of China grant (S2012010008368) and a startup fund from The First Affiliated Hospital of Sun Yat-sen University (to Z. Ma), and scholarships from the Chinese Scholarship Council (CSC). This research was also supported by the Radiation Resources Core Facility and Cytometry & Imaging Microscopy Core Facility of the Case Comprehensive Cancer Center (P30 CA43703). The work described was supported by a grant (R01CA154625) from the National Cancer Institute and seed grants from the Case Comprehensive Cancer Center and VeloSano Bike to Cure Foundation (to J. Zhang); a National Natural The authors apologize to colleagues whose work was not cited because of space limitations or ignorance. Our thanks for the service provided by BioMed Proofreading LLC. The work described was supported by a grant (R01CA154625) from the National Cancer Institute and seed grants from the Case Comprehensive Cancer Center and VeloSano Bike to Cure Foundation (to J. Zhang); a National Natural Science Foundation of China grant (31571452 and 31271503) and Guangdong Provincial Natural Science Foundation of China grant (S2012010008368) and a startup fund from The First Affiliated Hospital of Sun Yat-sen University (to Z. Ma), and scholarships from the Chinese Scholarship Council (CSC). This research was also supported by the Radiation Resources Core Facility and Cytometry & Imaging Microscopy Core Facility of the Case Comprehensive Cancer Center (P30 CA43703).
FundersFunding numbers
BioMed Proofreading LLC
-
Chinese Scholarship Council
-
First Affiliated Hospital of Sun Yat-sen University
-
Guangdong Provincial Natural Science Foundation of China
-
China Postdoctoral Science Foundation
-
VeloSano Bike to Cure Foundation
-
NCI
R01CA154625
NIGMS
R01GM107058
Case Comprehensive Cancer Center, Case Western Reserve University
-
NSFC
31271503, 31571452
SYSU
-
Natural Science Foundation of Guangdong Province
S2012010008368
CSC
P30 CA43703