Evidence map›Paper›PMID 35104452›Full record

ArticleMolecular cell2022

SPARCLE, a p53-induced lncRNA, controls apoptosis after genotoxic stress by promoting PARP-1 cleavage.

Karla F Meza-Sosa, Rui Miao, Francisco Navarro, Zhibin Zhang, Ying Zhang, Jun Jacob Hu, Corrine Corrina R Hartford, Xiao Ling Li, Gustavo Pedraza-Alva, Leonor Pérez-Martínez and 3 more

Open access · greenAbstract read
In one paragraph

Article in Molecular cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.1field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. iScience · 2026
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  5. Knockdown of caspase-activated DNase and B-cell lymphoma 2 inhibits cell proliferation and drug resistance in TP53-mutant multiple myeloma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. EGFR-induced lncRNAProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 2 countries.

Karla F Meza-SosaProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA; Laboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, MOR 62210, México. Electronic address: karla.meza@ibt.unam.mx.
Rui MiaoProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
Francisco NavarroProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA; Bluebird Bio, Cambridge, MA 02142, USA.
Zhibin ZhangProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
Ying ZhangProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
Jun Jacob HuProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115, USA; Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
Corrine Corrina R HartfordRegulatory RNAs and Cancer Section, Genetics Branch, Center for Cancer Research (CCR), National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD 20895, USA.
Xiao Ling LiRegulatory RNAs and Cancer Section, Genetics Branch, Center for Cancer Research (CCR), National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD 20895, USA.
Gustavo Pedraza-AlvaLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, MOR 62210, México.
Leonor Pérez-MartínezLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, MOR 62210, México.
Ashish LalRegulatory RNAs and Cancer Section, Genetics Branch, Center for Cancer Research (CCR), National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD 20895, USA.
Hao WuProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115, USA; Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
Judy LiebermanProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. Electronic address: judy.lieberman@childrens.harvard.edu.
Boston Children's Hospital · USNational Cancer Institute · USUniversidad Nacional Autónoma de México · MX

Funding

Role of long non-coding RNAs in p53 signalingZIABC011646 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LAL, ASHISH · 2015 to 2025
$15.0M
Novel Mechanisms of Disarming Anti-HIV Host Defenses by MethamphetamineR01DA039566 · NIDA · BETH ISRAEL DEACONESS MEDICAL CENTER · PI GROOPMAN, JEROME E · 2015 to 2019
$1.8M
Intramural NIH HHS ZIA BC011646NIDA NIH HHS R01 DA039566
6 · The paper itself

Abstract

p53, master transcriptional regulator of the genotoxic stress response, controls cell-cycle arrest and apoptosis following DNA damage. Here, we identify a p53-induced lncRNA suicidal PARP-1 cleavage enhancer (SPARCLE) adjacent to miR-34b/c required for p53-mediated apoptosis. SPARCLE is a ∼770-nt, nuclear lncRNA induced 1 day after DNA damage. Despite low expression (<16 copies/cell), SPARCLE deletion increases DNA repair and reduces DNA-damage-induced apoptosis as much as p53 deficiency, while its overexpression restores apoptosis in p53-deficient cells. SPARCLE does not alter gene expression. SPARCLE binds to PARP-1 with nanomolar affinity and causes apoptosis by acting as a caspase-3 cofactor for PARP-1 cleavage, which separates PARP-1's N-terminal (NT) DNA-binding domain from its catalytic domains. NT-PARP-1 inhibits DNA repair. Expressing NT-PARP-1 in SPARCLE-deficient cells increases unrepaired DNA damage and restores apoptosis after DNA damage. Thus, SPARCLE enhances p53-induced apoptosis by promoting PARP-1 cleavage, which interferes with DNA-damage repair.

Indexed as

ApoptosisDNA Breaks, Double-StrandedDNA Breaks, Single-StrandedA549 CellsAnimalsCaspase 3Colorectal NeoplasmsDNA RepairGene Expression Regulation, NeoplasticHCT116 CellsHEK293 CellsHep G2 CellsHumansMaleMiceMice, NudeCASP3 protein, humanCaspase 3MicroRNAsMIRN34 microRNA, humanPARP1 protein, humanPoly (ADP-Ribose) Polymerase-1RNA, Long NoncodingTP53 protein, humanTumor Suppressor Protein p53apoptosisgenotoxic stresslncRNAmiR-34p53PARP-1

Identifiers

PMID35104452
PMCPMC10392910
OpenAlexW4210681096

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.