Loss of TRIM33 in Multiple Myeloma correlates with increased genomic instability

McAvera, Roisin; Morgan, Jonathan J.; Johnston, Cliona K.; Mills, Ken; Crawford, Lisa

doi:10.1016/j.clml.2019.09.111

Cited by 1 publication

(2 citation statements)

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“…Analysis of human cancer cell lines and patient data revealed that reduced TRIM33 expression correlates with increased genomic rearrangements, further indicating that TRIM33 regulates chromosomal stability [33]. In agreement with these findings, we have similarly demonstrated that MM patients with loss of TRIM33 display an increased frequency of genomic rearrangements [60]. inactivation in TRIM33-deficient cells may also contribute to the higher endogenous damage observed in other studies.…”

Section: Trim33 Regulation Of Mitotic Checkpointssupporting

confidence: 88%

“…Furthermore, shRNA knockdown of TRIM33 in HeLa cells lead to increased basal γH2AX, phosphorylated Chk2 and heightened sensitivity to bleomycin, a chemotherapeutic agent that induces single and double strand DNA breaks [59]. Similarly, we have shown that multiple myeloma cell lines with low TRIM33 expression have higher endogenous DNA damage as assessed by γH2AX levels [60]. TRIM33 is also required for the recruitment of CBX8 to sites of damage, another PARP-dependent DDR protein involved in both HR and NHEJ [61].…”

Section: Localisation Of Tif1 Proteins To Sites Of Dna Damagementioning

confidence: 60%

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TIF1 Proteins in Genome Stability and Cancer

McAvera

Crawford

2020

Cancers

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Genomic instability is a hallmark of cancer cells which results in excessive DNA damage. To counteract this, cells have evolved a tightly regulated DNA damage response (DDR) to rapidly sense DNA damage and promote its repair whilst halting cell cycle progression. The DDR functions predominantly within the context of chromatin and requires the action of chromatin-binding proteins to coordinate the appropriate response. TRIM24, TRIM28, TRIM33 and TRIM66 make up the transcriptional intermediary factor 1 (TIF1) family of chromatin-binding proteins, a subfamily of the large tripartite motif (TRIM) family of E3 ligases. All four TIF1 proteins are aberrantly expressed across numerous cancer types, and increasing evidence suggests that TIF1 family members can function to maintain genome stability by mediating chromatin-based responses to DNA damage. This review provides an overview of the TIF1 family in cancer, focusing on their roles in DNA repair, chromatin regulation and cell cycle regulation.

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Section: Trim33 Regulation Of Mitotic Checkpointssupporting

confidence: 88%