Evidence map›Paper›PMID 39107463›Full record

ReviewOncogene2024

RHNO1: at the crossroads of DNA replication stress, DNA repair, and cancer.

Niphat Jirapongwattana, Samuel F Bunting, Donald R Ronning, Gargi Ghosal, Adam R Karpf

Abstract readReview
In one paragraph

Review in Oncogene, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
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

5 authors.

Niphat JirapongwattanaEppley Institute for Research in Cancer, University of Nebraska Medical Center, Omaha, NE, 68198-6805, USA.
Samuel F BuntingDepartment of Molecular Biology and Biochemistry, Rutgers, The State University of New Jersey, Piscataway, NJ, 08854-8021, USA.
Donald R RonningDepartment of Pharmaceutical Sciences, University of Nebraska Medical Center, Omaha, NE, 68198-6805, USA.
Gargi GhosalFred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, 68198-6805, USA.
Adam R KarpfEppley Institute for Research in Cancer, University of Nebraska Medical Center, Omaha, NE, 68198-6805, USA. adam.karpf@unmc.edu.ORCID 0000-0002-0866-0666

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Tracie Saunders · 1997 to 2026
$94.5M
UNMC/EPPLEY CANCER CENTER SUPPORT GRANTP30CA036727 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI James Eudy · 1985 to 2026
$55.0M
Project 4: The BRCA Network in Medulloblastoma Responses to Replication StressP01CA250957 · NCI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI DE, SUBHAJYOTI · 2021 to 2025
$11.3M
Rutgers Mass Spectrometry Core for Integrative Neuroscience ResearchP30NS046593 · NINDS · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI LOBEL, PETER · 2004 to 2018
$9.9M
Mechanisms underlying USP1-mediated bypass of EWS-FLI1 oncogene-induced replication stress in Ewing sarcomaR01CA263504 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI GARGI GHOSAL · 2022 to 2026
$1.7M
Regulation of SPRTN protease and SPRTN-mediated DNA-Protein Crosslink RepairR01GM141232 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI GHOSAL, GARGI · 2022 to 2025
$1.3M
Targeting RHNO1 in Ovarian CancerR21CA273399 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI KARPF, ADAM R. · 2023 to 2024
$384k
NCI NIH HHS P01 CA250957NCI NIH HHS P30 CA036727NCI NIH HHS P30 CA072720NCI NIH HHS R01 CA263504NCI NIH HHS R21 CA273399NIGMS NIH HHS R01 GM141232NINDS NIH HHS P30 NS046593
6 · The paper itself

Abstract

The DNA replication stress (DRS) response is a crucial homeostatic mechanism for maintaining genome integrity in the face of intrinsic and extrinsic barriers to DNA replication. Importantly, DRS is often significantly increased in tumor cells, making tumors dependent on the cellular DRS response for growth and survival. Rad9-Hus1-Rad1 Interacting Nuclear Orphan 1 (RHNO1), a protein involved in the DRS response, has recently emerged as a potential therapeutic target in cancer. RHNO1 interacts with the 9-1-1 checkpoint clamp and TopBP1 to activate the ATR/Chk1 signaling pathway, the crucial mediator of the DRS response. Moreover, RHNO1 was also recently identified as a key facilitator of theta-mediated end joining (TMEJ), a DNA repair mechanism implicated in cancer progression and chemoresistance. In this literature review, we provide an overview of our current understanding of RHNO1, including its structure, function in the DRS response, and role in DNA repair, and discuss its potential as a cancer therapeutic target. Therapeutic targeting of RHNO1 holds promise for tumors with elevated DRS as well as tumors with DNA repair deficiencies, including homologous recombination DNA repair deficient (HRD) tumors. Further investigation into RHNO1 function in cancer, and development of approaches to target RHNO1, are expected to yield novel strategies for cancer treatment.

Indexed as

DNA RepairDNA ReplicationNeoplasmsAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCheckpoint Kinase 1DNA-Binding ProteinsDNA DamageHumansNuclear ProteinsSignal TransductionAtaxia Telangiectasia Mutated ProteinsATR protein, humanCell Cycle ProteinsCheckpoint Kinase 1CHEK1 protein, humanDNA-Binding ProteinsNuclear Proteins

Identifiers

PMID39107463
PMCPMC13390501

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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 Socratic graph.