Correction: WRAP53 Is Essential for Cajal Body Formation and for Targeting the Survival of Motor Neuron Complex to Cajal Bodies

Mahmoudi, Salah; Henriksson, Sofia; Weibrecht, Irene; Smith, Stephen A.; Söderberg, Ola; Strömblad, Staffan; Wiman, Klas G.; Farnebo, Marianne

doi:10.1371/journal.pbio.3000030

Cited by 4 publications

(2 citation statements)

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“…The WRAP53-1β transcript is not complementary to TP53 but encodes the WD repeat-containing protein WRAP53β (WD repeat domain 79) and telomerase Cajal body protein 1, which is involved in multiple cellular processes. WRAP53β regulates the maintenance of the nuclear organelles known as Cajal bodies by recruiting motor neuron proteins, small Cajal body-specific RNAs, and telomerases [9][10][11]. WRAP53β also targets telomerase to telomeres, promoting their elongation [9].…”

Section: Introductionmentioning

confidence: 99%

Differential effects of WRAP53 transcript variants on non-small cell lung cancer cell behaviors

et al. 2023

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Background The WD40-encoding RNA antisense to p53 (WRAP53) is an antisense gene of TP53 with three transcriptional start sites producing three transcript variants involved in the progression of non-small cell lung cancer. However, the mechanism by which these different transcript variants regulate non-small cell lung cancer cell behaviors is to be elucidated. Methods Two non-small cell lung cancer cell lines, A549 cells with wild-type p53 and H1975 with mutated p53, were transfected with WRAP53-1α and WRAP53-1β siRNA. The biological effects were assessed via colony formation, cell viability, apoptosis, cell cycle, wound healing and cell invasion assays, as well as immunoblotting. Results Knockdown of WRAP53-1α increased the mRNA and protein levels of p53; suppressed colony formation and proliferation of A549 cells but promoted them in H1975 cells; increased the proportion of cells in the G0/G1 phase in A549 cells but decreased that in H1975 cells; and suppressed migration and invasion in A549 cells but not in H1975 cells. Conversely, knockdown of WRAP53-1β had no effect on p53 expression; promoted the growth of A549 cells but not of H1975 cells; decreased the proportion of cells in the G0/G1 phase in A549 cells but not in H1975 cells; and promoted migration and invasion in A549 cells but not in H1975 cells. Knockdown of both WRAP53-1α and WRAP53-1β promoted apoptosis in A549 cells but not in H1975 cells. Conclusions WRAP53 transcript variants exerted different functions in non-small cell lung cancer cells and regulated non-small cell lung cancer cell behaviors depending on the p53 expression.

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Section: Introductionmentioning

confidence: 99%

Differential effects of WRAP53 transcript variants on non-small cell lung cancer cell behaviors

et al. 2023

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“…The WRAP53-1β transcript is not complementary to TP53, but encodes the WD repeat-containing protein WRAP53β, also known as WD repeat domain 79 and telomerase Cajal body protein 1, which is involved in multiple cellular processes. WRAP53β was reported to regulate the maintenance of the nuclear organelles known as Cajal bodies via recruiting motor neuron proteins, small Cajal body-speci c RNAs, and telomerases [9][10][11]. WRAP53β also targeted telomerase to telomeres, promoting their elongation [9].…”

Section: Introductionmentioning

confidence: 99%

Differential Effects of WRAP53 Transcript Variants on the Biological Behaviours of Human Non-Small Cell Lung Cancer Cells

Zhu

Sun

Jiang

et al. 2021

Preprint

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Background: The WD40-encoding RNA antisense to p53 (WRAP53) gene, an antisense gene of TP53, has 3 different transcriptional start sites that yield 3 transcript variants. One of these variants WRAP53-1β encodes a WD repeat-containing protein WRAP53β, whereas WRAP53-1α is a noncoding RNA that regulates p53 mRNA levels. These variants are involved in the progression of non-small cell lung cancer (NSCLC). However, how the different transcript variants regulate NSCLC cell behaviours is to be elucidated.Methods: Wild-type p53 NSCLC A549 cells and p53-mutated H1975 cells were transfected with WRAP53-1α and WRAP53-1β siRNAs, and their behaviours were examined colony formation, cell viability, apoptosis, cell cycle, wound healing, and cell invasion assays.Results: WRAP53-1α knockdown increased the mRNA and protein levels of p53, whereas depletion of WRAP53-1β had no effect on p53 expression. WRAP53-1α knockdown suppressed colony formation and proliferation of A549 cells, but had the opposite effects on H1975 cells. However, WRAP53-1β knockdown promoted A549 cell growth. Depletion of WRAP53-1α and WRAP53-1β promoted apoptosis in A549 but not H1975 cells. WRAP53-1α knockdown increased the proportion of A549 but not H1975 cells at the G0/G1 phase. However, WRAP53-1β knockdown decreased the proportion of cells at the G0/G1 phase in A549 cells. Depletion of WRAP53-1α suppressed A549 cell migration and invasion, and promoted H1975 cell migration and invasion. However, depletion of WRAP53-1β had the opposite effects.Conclusions: The 2 WRAP53 transcript variants exerted opposite functions in NSCLC cells and regulated NSCLC cell behaviours in a p53-dependent manner.

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UHMK1-dependent phosphorylation of Cajal body protein coilin alters 5-FU sensitivity in colon cancer cells

et al. 2022

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Resistance to 5-fluorouracil (5-FU) in chemotherapy and recurrence of colorectal tumors is a serious concern that impedes improvements to clinical outcomes. In the present study, we found that conditioned medium (CM) derived from 5-FU-resistant HCT-8/FU cells reduced 5-FU chemosensitivity in HCT-8 colon cancer cells, with corresponding changes to number and morphology of Cajal bodies (CBs) as observable nuclear structures. We found that U2AF homology motif kinase 1 (UHMK1) altered CB disassembly and reassembly and regulated the phosphorylation of coilin, a major component of CBs. This subsequently resulted in a large number of variations in RNA alternative splicing that affected cell survival following 5-FU treatment, induced changes in intracellular phenotype, and transmitted preadaptive signals to adjacent cells in the tumor microenvironment (TME). Our findings suggest that CBs may be useful for indicating drug sensitivity or resistance in tumor cells in response to stress signals. The results also suggest that UHMK1 may be an important factor for maintaining CB structure and morphology by regulating splicing events, especially following cellular exposure to cytotoxic drugs. Graphical Abstract

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Correction: WRAP53 Is Essential for Cajal Body Formation and for Targeting the Survival of Motor Neuron Complex to Cajal Bodies

Cited by 4 publications

References 1 publication

Differential effects of WRAP53 transcript variants on non-small cell lung cancer cell behaviors

Differential effects of WRAP53 transcript variants on non-small cell lung cancer cell behaviors

Differential Effects of WRAP53 Transcript Variants on the Biological Behaviours of Human Non-Small Cell Lung Cancer Cells

UHMK1-dependent phosphorylation of Cajal body protein coilin alters 5-FU sensitivity in colon cancer cells

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