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Cited by 39BRCA gene mutations in cancerDNA Repair MechanismsCancer-related Molecular Pathways

The BRCA1-Interacting Protein Abraxas Is Required for Genomic Stability and Tumor Suppression

Open access
Castillo, Andy, Paul, Atanu, Sun, Baohua, Huang, Ting Hsiang, Wang, Yucai, Yazinski, Stephanie A., Tyler, Jessica, Li, Lei +4 more·2014·Cell Reports
DOI 10.1016/j.celrep.2014.06.050PMC PMC4149256
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Abstract

Germline mutations of BRCA1 confer hereditary susceptibility to breast and ovarian cancer. However, somatic mutation of BRCA1 is infrequent in sporadic breast cancers. The BRCA1 protein C terminus (BRCT) domains interact with multiple proteins and are required for BRCA1's tumor-suppressor function. In this study, we demonstrated that Abraxas, a BRCA1 BRCT domain-interacting protein, plays a role in tumor suppression. Abraxas exerts its function through binding to BRCA1 to regulate DNA repair and maintain genome stability. Both homozygous and heterozygous Abraxas knockout mice exhibited decreased survival and increased tumor incidence. The gene encoding Abraxas suffers from gene copy loss and somatic mutations in multiple human cancers including breast, ovarian, and endometrial cancers, suggesting that mutation and loss of function of Abraxas may contribute to tumor development in human patients.

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Crossref · 10.1016/j.celrep.2014.06.050

Cites

34 of 34 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 30 cited sources checked · 0 supported · 0 flagged

  • Findingown data

    Full-length Abraxas protein is lost in AbraxasΔ/Δ MEFs.

    “The loss of Abraxas full-length protein was also confirmed in AbraxasΔ/Δ MEFs by immunoblotting (Figure 1B and S1) with an antibody recognizing the C-terminus region of the mouse Abraxas protein.”
    Quote in the paperSubstantial claim
  • Findingown data

    Abraxas-/- cells show reduced sister chromatid exchanges per metaphase compared with wild-type cells.

    “Compared to wild type cells Abraxas-/- cells showed reduced sister chromatid exchanges per metaphase (Figure 2C)”
    Quote in the paperSubstantial claim
  • Findingnone given

    The Abraxas gene shows copy loss and somatic mutations in multiple human cancers, including breast, ovarian, and endometrial cancers.

    “The gene encoding Abraxas suffers from gene copy loss and somatic mutations in multiple human cancers including breast, ovarian, and endometrial cancers”
    Quote in the paperSubstantial claim
  • Findingown data

    MEF cells from Abraxas-/- mice have increased sensitivity to IR, mitomycin C, and olaparib.

    “Similarly, MEF cells prepared from Abraxas-/- mice displayed increased sensitivity to IR, the DNA crosslinking agent mytomycin C (MMC) and poly ADP ribose polymerase (PARP) inhibitor Olaparib (Figure 1D).”
    Quote in the paperSubstantial claim
  • Findingown data

    Abraxas mutants failed to rescue the DNA repair deficiency of Abraxas-/- cells in the comet assay.

    “The mutants also failed to rescue the DNA repair deficiency of Abraxas-/- cells using a comet assay to assess DNA repair efficiency (Figure 2F).”
    Quote in the paperSubstantial claim
  • May combine two claims. 33
  • Classified as probably not a substantial claim. 12

  • May combine two claims.

    Findingown data

    Abraxas-/- cells have a higher percentage of unrepaired DNA, with increased tail moments, at 6 hours after IR in the comet assay.

    “Compared to wild type cells, Abraxas-/- cells appeared to have much higher percentage of cells having unrepaired DNA (increased tail moments) at 6 hour post IR treatment (Figure 2B and S2).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Abraxas-/- mice show no gross developmental defects and are indistinguishable from wild-type littermates after birth.

    “Abraxas-/- (AbraxasΔ/Δ) mice did not exhibit any gross developmental defects and were indistinguishable from their wild type littermates after birth.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    AbraxasΔ/Δ mice are viable and born at expected Mendelian ratios.

    “Intercrossing of Abraxas+/Δ mice indicated that AbraxasΔ/Δ mice were viable and born at expected Mendelian ratios.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    The exon 5-deleted Abraxas transcript contains a premature stop codon and likely undergoes nonsense-mediated decay, as indicated by decreased transcript levels.

    “Sequencing of the RT-PCR products spanning exon 2 to exon 6 confirmed that the exon 5-deleted transcript contains a premature STOP codon and has likely undergone nonsense mediated decay indicated by decreased transcript levels (Figure S1).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Abraxas-/- MEFs are defective in DNA repair, as shown by persistent γH2AX foci after IR.

    “the Abraxas-/- cells, however, consistently displayed a high percentage of cells with γH2AX foci through the duration of the experiment indicating a deficiency in DNA repair (Figure 2A).”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Findingown data

    BRCA1-deficient Brca1Δ11/Δ11 MEFs are also defective in DNA repair in the comet assay.

    “As a comparison, BRCA1-deficient Brca1Δ11/Δ11 MEF cells were also defective in DNA repair in the comet assay (Figure S2).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    After 7.5 Gy IR, most Abraxas-/- mice died between 7 and 28 days, whereas no wild-type mice died in that period.

    “After treatment, the majority of Abraxas-/- mice died between 7-28 days post irradiation, while none of the wild type mice died during this same time frame (Figure 1C).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Both homozygous and heterozygous Abraxas knockout mice had reduced survival and increased tumor incidence.

    “Both homozygous and heterozygous Abraxas knockout mice exhibited decreased survival and increased tumor incidence.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Tumors were detected in some Abraxas+/- or Abraxas-/- mice as early as 8 months, and the mean age of tumor development was 17 months for Abraxas-/- and 24 months for Abraxas+/- mice.

    “Although tumors were detected in some Abraxas+/- or Abraxas-/- mice as early as 8 months of age, the mean age of Abraxas-/- and Abraxas+/- mice that developed tumor was 17 months and 24 months respectively.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    IR-treated Abraxas-/- MEFs show multiple breaks per metaphase and significant increases in chromosomal fusions and radial structures, whereas wild-type aberrations are mostly single breaks and rarely fusions or radial structures.

    “while chromosomal aberrations in wild type cells are mostly single breaks and very rarely fusions and radial structures, IR treated Abraxas-/- MEFs manifested multiple breaks per metaphase as well as significant increases in chromosomal fusion events and radial structures (Figure 5C and 5D).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingnone given

    Abraxas seems unnecessary for ubiquitination of FancD2 and for its recruitment to crosslink lesions.

    “Since Abraxas does not appear to be required for FancD2 ubiquitination and recruitment to crosslink damage sites”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Abraxas+/- and Abraxas-/- mice have significantly reduced life span and decreased disease-free survival compared with wild-type mice.

    “Compared to wild-type mice, Abraxas+/- and Abraxas-/- mice had a significantly reduced life span exhibiting decreased disease-free survival (Figure 6A).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Gene copy number loss of the Abraxas locus at chromosome 4q21 is frequent in ovarian, breast (especially basal subtype), lung, and colon cancers, and involves loss of the whole chromosome 4q arm.

    “Gene copy number loss of the Abraxas locus at chromosome 4q21 is frequently found in ovarian, breast (especially basal subtype), lung, and colon cancers, which involves the loss of whole chromosome 4q arm (Figure 7B and Supplemental Table S1).”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Findingnone given

    Abraxas is not required for stalled replication fork protection.

    “Abraxas, unlike BRCA1, is not required for embryonic development or stalled replication fork protection.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Abraxas interacts with FancD2 in co-immunoprecipitation assays, and this interaction is not induced by IR or MMC.

    “In addition, Abraxas interacted with FancD2 in co-immunoprocipitation assays and the interaction appeared not to be induced by DNA damaging agents such as IR or MMC treatment (Figure 4B).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingnone given

    Abraxas shows lower expression, copy-number loss, and mutation across several human tumor types, including breast and ovarian cancer.

    “In addition, reduced expression, gene copy loss and mutation of Abraxas are also observed in multiple types of human tumor including breast and ovarian cancer.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Among 26 non-synonymous Abraxas mutations, five nonsense mutations and one frame-shift insertion generate truncated or abnormal protein products that lack the pSPxF motif and cannot bind BRCA1.

    “Among all 26 non-synonymous mutations found in Abraxas, five nonsense mutations and one frame-shift insertion were found to generate truncated or abnormal protein products that lack the pSPxF motif and incapable of binding to the BRCA1 protein.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Abraxas-deficient cells had more spontaneous breaks and more IR-induced chromosomal abnormalities than wild-type cells, including multiple breaks, fusions, and radial forms.

    “compared to wild type cells, Abraxas-/- cells displayed increased spontaneous breaks and IR induced chromosome aberrations including multiple breaks, fusions and radial structures.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Mice lacking Abraxas survive and appear at the expected Mendelian frequency.

    “Abraxas null mice are viable and born at expected Mendelian ratios”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Abraxas is not required for FancD2 foci formation or FancD2 ubiquitination after MMC treatment in human cells treated with Abraxas shRNAs.

    “We found that Abraxas is not required for FancD2 foci formation or ubiquitination in response to MMC treatment (Figure S4).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Somatic mutations of Abraxas occur in endometrial, colon, lung, liver, kidney cancers and leukemia, with the highest mutation rate in endometrial cancer at 2.5%.

    “Furthermore, somatic mutations of Abraxas are found in endometrial, colon, lung, liver, kidney cancers, and in leukemia (Supplemental Table S1 and S2) with the highest mutation rate found in endometrial cancer (2.5%).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Tumor samples from Abraxas+/- mice retained the wild-type allele and expressed Abraxas.

    “The tumor samples analyzed appeared to retain the wild type allele and expression of Abraxas indicating the remaining wild-type allele is expressed (Figure S7)”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Mice with no or one functional Abraxas allele develop tumors at a high rate, exceeding 60%, mostly lymphomas and other tumor types.

    “Both Abraxas null and heterozygous mice are tumor prone with over 60% tumor incidence developing lymphomas and other tumors.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    IR-induced chromosome aberrations in Abraxas null cells are greatly reduced by wild-type Abraxas but not by the S404A mutant defective in BRCA1 interaction.

    “The IR-induced chromosome aberrations in Abraxas null cell were greatly reduced when the null cells were complemented with expression of wild type Abraxas but not with the S404A mutant that is defective in interacting with BRCA1.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Mice without Abraxas are hypersensitive to ionizing radiation, and Abraxas-deficient MEFs are hypersensitive to agents including IR, MMC, and PARPi.

    “In addition, lack of Abraxas in mice results in hypersensitivity of mice to IR and MEF cells to DNA damaging agents such as IR, MMC and PARPi.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Rap80 interacts with FancD2, and this interaction is independent of DNA damage.

    “Rap80, another component in the BRCA1-A complex also interacted with FancD2, and similarly, the interaction was independent of DNA damage (Figure S4).”
    Quote in the paperNot a substantial claim

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    Mice carrying a BRCA1 BRCT mutant defective in phosphoprotein recognition are prone to tumors, indicating that BRCT phosphoprotein recognition is required for BRCA1 tumor suppression.

    “Mice carrying a BRCT mutant of BRCA1 defective in recognition of phosphorylated proteins are prone to tumor development indicating that BRCT phosphoprotein recognition is required for BRCA1 tumor suppression (Shakya et al., 2011).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Shakya et al., 2011 source

      Not checked in the free run.

  • May combine two claims.

    Interpretationown data

    Interaction of Abraxas with BRCA1, and formation of the BRCA1-A complex, is critical for efficient DNA repair.

    “Together, these results indicate that the interaction of Abraxas with BRCA1, as well as the formation of the BRCA1-A complex, is critical for efficient DNA repair.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).

    Premisenone given

    Abraxas dimerizes with BRCC36 through a coiled-coil domain present on both proteins.

    “In addition, Abraxas dimerizes with BRCC36 through a coiled-coil domain present on both proteins.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    Abraxas, Bach1, and CtIP directly interact with BRCA1 BRCT domains through the pSPxF motif in a phosphorylation-dependent manner, forming mutually exclusive A, B, and C complexes.

    “Three proteins, Abraxas (also known as Abra1, FAM175A, CCDC98), Bach1 (also known as Brip1, FancJ) and CtIP (also known as RBBP8), directly interact with the BRCA1 BRCT domains through the pSPxF motif in a phosphorylation-dependent manner forming mutually exclusive complexes, which were thus named as the A, B and C complexes of BRCA1 (Greenberg et al., 2006; Kim et al., 2007; Liu et al., 2007;”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites Greenberg et al., 2006 source

      Not checked in the free run.

    • cites Kim et al., 2007 source

      Not checked in the free run.

    • cites Liu et al., 2007 source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    BRCT domains are frequently affected by clinically important mutations, and most of these mutations disrupt the BRCT domain's phosphopeptide-binding surface.

    “BRCT domains are frequently targeted by many clinically important mutations and most of these mutations disrupt the binding surface of the BRCT domains to phosphorylated peptides (Bouwman et al., 2013; Glover, 2006).”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites Bouwman et al., 2013 source

      Not checked in the free run.

    • cites Glover, 2006 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Abraxas is a central adaptor protein in the BRCA1 A complex and contains domains needed for interactions with BRCA1 and other complex components.

    “In the BRCA1 A complex, Abraxas appears to be a central adaptor protein, as it harbors several domains necessary for the interactions with BRCA1 and other components in the complex (Wang, 2012).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Wang, 2012 source

      Not checked in the free run.

  • Classified as probably not a substantial claim.

    Premisecitation

    The C-terminal BRCT domains of BRCA1 form a phospho-peptide recognition domain that specifically binds phospho-peptides containing a pSPxF motif.

    “The C-terminal BRCT domains of BRCA1 constitute a phospho-peptide recognition domain that binds specifically to phospho-peptides containing a pSPxF (phosphor-serine-proline-x-phenylalanine) motif (Manke et al., 2003; Rodriguez et al., 2003; Yu et al., 2003).”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites Manke et al., 2003 source

      Not checked in the free run.

    • cites Rodriguez et al., 2003 source

      Not checked in the free run.

    • cites Yu et al., 2003

      Not checked in the free run.

  • Classified as probably not a substantial claim.

    Premisecitation

    BRCA1 is implicated in a repair-independent mechanism that protects stalled replication forks from degradation.

    “BRCA1 is implicated in a repair-independent mechanism in protecting stalled replication forks from degradation to maintain genome stability (Schlacher et al., 2012).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Schlacher et al., 2012 source

      Not checked in the free run.

  • Classified as probably not a substantial claim.

    Premisecitation

    BRCA1-deficient cells show significant shortening of fork length after hydroxyurea treatment, indicating degradation of stalled replication forks.

    “As previously shown, BRCA1-deficient cells show significant shortening of fork length following hydroxyurea (HU) treatment indicating degradation of stalled replication forks.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Schlacher et al., 2012 source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisenone given

    The N-terminus of Abraxas, including its MPN domain, is important for interactions with NBA1, BRE, and Rap80.

    “The N-terminus of Abraxas including a MPN domain is important for interactions with NBA1, BRE and Rap80.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Interpretationreasoning

    Abraxas does not participate in all functions of BRCA1.

    “However, it is also not surprising that Abraxas does not participate in all the function of BRCA1.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationreasoning

    Abraxas is important in BRCA1 signaling and accounts for part of BRCA1's contribution to DSB repair and genome stability.

    “This is consistent with Abraxas plays an important role in BRCA1 signaling, mediating at least partly of BRCA1's role in double strand break repair and maintaining genome stability.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    In mice, the genetic background affects which tumor type appears and how long it takes.

    “it is known that genetic background plays a role in both the type of tumor that develops and tumor latency in mice (Donehower and Lozano, 2009).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Donehower and Lozano, 2009

      Not checked in the free run.

  • May combine two claims.

    Interpretationreasoning

    Abraxas contributes to BRCA1 signaling for DNA repair and genome stability, and probably for tumor suppression too.

    “Thus, Abraxas is part of the BRCA1 signaling in DNA repair, maintenance of genome stability and likely tumor suppression as well.”
    • Also stated in: § Discussion · hedged
      “It is also likely to be part of the BRCA1 signaling that contributes to tumor suppression.”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    BRCA1 interacts with FancD2 and mediates FancD2 foci formation after mitomycin C treatment.

    “Since BRCA1 interacts with FancD2 and mediates FancD2 foci formation after treatment with MMC (Bunting et al., 2012; Garcia-Higuera et al., 2001; Vandenberg et al., 2003)”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites Bunting et al., 2012 source

      Not checked in the free run.

    • cites Garcia-Higuera et al., 2001 source

      Not checked in the free run.

    • cites Vandenberg et al., 2003 source

      Not checked in the free run.

41 of 41

  • The authors state this as an assumption.

    Before this study, the role of Abraxas in DNA repair, BRCA1 signaling, and tumor suppression was not clear.

    “However it's role in DNA repair, BRCA1 signaling and tumor suppression is not clear.”

  • The paper relies on this without support.

    In breast and ovarian cancer, somatic BRCA1 mutation rate is low.

    “In breast cancer and ovarian cancer, somatic BRCA1 mutation rate is low.”

  • The paper relies on this without support.

    Abraxas and its partner Rap80 bind FancD2 and localize to crosslink lesions.

    “Both Abraxas and its interacting protein Rap80 interact with FancD2 and are recruited to DNA crosslink damage sites”

  • The paper relies on this without support.

    Their recruitment to crosslink lesions requires stalled replication forks.

    “the recruitment appears to depend on the presence of stalled replication forks”
4 of 4

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • The 4 patients with deficiencies in BRCA1-binding proteins BARD1, BRIP1, FAM175A and FANCA were all predicted as having BRCA1-type HRD.

    “Likewise, the 4 patients with deficiencies in the BRCA1-binding proteins, BARD124 (n = 1), BRIP125 (n = 1), FAM175A26 (n = 1) and FANCA27 (n = 1), were all predicted as having BRCA1-type HRD.”

    From Pan-cancer landscape of homologous recombination deficiency. (2020) · cites this paper as [26]

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Authors
Castillo, A., Paul, A., Sun, B., Huang, T. H., Wang, Y., Yazinski, S. A., Tyler, J., Li, L., You, M. J., Zou, L., Yao, J., & Wang, B.
Affiliations
  • The University of Texas MD Anderson Cancer Center (US)
  • Harvard University (US)
Corresponding author
Wang, Bin
ORCID
Venue
Cell Reports
Publisher
Elsevier BV
Published
2014-08
Volume
8
Issue
3
Pages
807-817
ISSN
2211-1247 (ISSN-L)
DOI
10.1016/j.celrep.2014.06.050
PMC
PMC4149256
OpenAlex
W2069400465
Cited by
39
References
34
Citations by year
2026: 3 · 2025: 2 · 2024: 2 · 2023: 1 · 2022: 1 · 2021: 2 · 2020: 6 · 2019: 5 · 2018: 2 · 2017: 4 · 2016: 8 · 2015: 2 · 2014: 1
FWCI
3.28
Type
journal article
Language
en
Open access
Licence
Locations
  • Cell Reports (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
National Cancer Institute (P50CA100632, R21CA179441, CA 009299, T32CA009299, R01CA095641, R01CA164346, R01CA155025, CA179441, CA127945, R01CA127945, CA155025, CA164346, P30CA016672)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Keywords
Abraxas, BRCA1, BRCT domain, tumor suppression, genome stability, DNA repair, somatic mutations, breast cancer, ovarian cancer, endometrial cancer, knockout mice, tumor incidence
MeSH terms
Animals, Breast Neoplasms, Carrier Proteins, DNA Repair, Female, Homozygote, Humans, Ovarian Neoplasms, Protein Binding, 3T3 Cells, Protein Structure, Tertiary, Germ-Line Mutation, BRCA1 Protein, Genomic Instability, Mice, HEK293 Cells

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