Detection of a deletion at 22q11 locus involving <i>ZNF280A/ZNF280B/PRAME/GGTLC2</i> in B‐cell malignancies: simply a consequence of an immunoglobulin lambda light chain rearrangement

Mráz, Marek; Pospı́šilová, Šárka

doi:10.1111/bjh.15922

Cited by 3 publications

(3 citation statements)

References 11 publications

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“…3) [75]. This resembles our previous observations describing the rearrangement of specific immunoglobulin light chain variable subgenes in B cells leading to miRNA production from the immunoglobulin transcript [88][89][90]. This has consequences for the biology of these cells, but it is unclear how this developed during immunoglobulin light chain gene evolution.…”

Section: Lncrnas In B Cell Activation and Differentiationsupporting

confidence: 82%

LncRNAs in adaptive immunity: role in physiological and pathological conditions

Zeni

Mráz

2020

RNA Biology

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The adaptive immune system is responsible for generating immunological response and immunological memory. Regulation of adaptive immunity including B cell and T cell biology was mainly understood from the protein and microRNA perspective. However, long non-coding RNAs (lncRNAs) are an emerging class of non-coding RNAs (ncRNAs) that influence key factors in lymphocyte biology such as NOTCH, PAX5, MYC and EZH2. LncRNAs were described to modulate lymphocyte activation by regulating pathways such as NFAT, NFκB, MYC, interferon and TCR/BCR signalling (NRON, NKILA, BCALM, GAS5, PVT1), and cell effector functions (IFNG-AS1, TH2-LCR). Here we review lncRNA involvement in adaptive immunity and the implications for autoimmune diseases (multiple sclerosis, inflammatory bowel disease, rheumatoid arthritis) and T/B cell leukaemias and lymphomas (CLL, MCL, DLBCL, T-ALL). It is becoming clear that lncRNAs are important in adaptive immune response and provide new insights into its orchestration.

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Section: Lncrnas In B Cell Activation and Differentiationsupporting

confidence: 82%

LncRNAs in adaptive immunity: role in physiological and pathological conditions

Zeni

Mráz

2020

RNA Biology

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“…However, our understanding about the biological role of ZNF280A in cancers is far from enough. The correlation between ZNF280A and hematologic malignancies has been previously reported ( 22 – 24 ). Their studies showed that the function of ZNF280A was correlated with deletions of chromosome 22q11.…”

Section: Discussionsupporting

confidence: 56%

Downregulation of ZNF280A inhibits proliferation and tumorigenicity of colorectal cancer cells by promoting the ubiquitination and degradation of RPS14

et al. 2022

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Colorectal cancer (CRC), one of the cancers with highest mortality, involves complicated molecular mechanisms leading to the onset of malignant phenotypes. ZNF280A, a member of the zinc-finger protein family, was shown to be a promotor of oncogenesis in CRC in this study. ZNF280A was remarkably upregulated in CRC tissues, which was meaningfully associated with tumor progression and poor prognosis in patients with CRC. Loss-of-function studies revealed that ZNF280A knockdown inhibited the development and progression of CRC as evident by the inhibition of cell proliferation, colony formation, cell apoptosis, cell cycle distribution, and cell migration in vitro and the repressed tumorigenesis of CRC cells in vivo. Next, we showed that RPS14 was the downstream target of ZNF280A and ZNF280A knockdown promoted the ubiquitination as well as degradation of RPS14 in CRC. Additionally, we demonstrated that RPS14 regulated the development of CRC via PI3K-Akt signaling pathway. Taken together, our findings provide a novel clear insight into ZNF280A/RPS14/PI3K-Akt axis in CRC for the first time, offering a potential target for early detection, diagnosis and treatment of CRC in future clinical applications.

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“…In particular, we demonstrate that PRAME deletions are independently associated with outcomes in multivariable analysis, making it unlikely that PRAME deletions are a pure surrogate for the prognostic effects of Ig-λ usage. As described by Mraz and Pospisilova, the association of PRAME deletion and Ig-λ rearrangement and expression is not absolute, and PRAME deletion is likely dependent on the exact V segment usage ( 3 ). Consistently, we did not observe PRAME deletions in the majority of patients expressing Ig-λ, and, interestingly, a minority of patients with PRAME deletions expressed Ig-κ.…”

Section: The Authors Replymentioning

confidence: 96%

Genetic mechanism for the loss of PRAME in B cell lymphomas. Reply.

Takata¹

2022

Journal of Clinical Investigation

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Detection of a deletion at 22q11 locus involving ZNF280A/ZNF280B/PRAME/GGTLC2 in B‐cell malignancies: simply a consequence of an immunoglobulin lambda light chain rearrangement

Cited by 3 publications

References 11 publications

LncRNAs in adaptive immunity: role in physiological and pathological conditions

LncRNAs in adaptive immunity: role in physiological and pathological conditions

Downregulation of ZNF280A inhibits proliferation and tumorigenicity of colorectal cancer cells by promoting the ubiquitination and degradation of RPS14

Genetic mechanism for the loss of PRAME in B cell lymphomas. Reply.

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