Evidence map›Paper›PMID 30082712›Full record

ArticleNature communications2018

NOVA1 regulates hTERT splicing and cell growth in non-small cell lung cancer.

Andrew T Ludlow, Mandy Sze Wong, Jerome D Robin, Kimberly Batten, Laura Yuan, Tsung-Po Lai, Nicole Dahlson, Lu Zhang, Ilgen Mender, Enzo Tedone and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

59 citing papers in PubMed, 84 citations in OpenAlex.

  1. Review
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  10. Splicing Factor PQBP1 Curtails BAX Expression to Promote Ovarian Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  11. Article
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  14. Review
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  16. Review
  17. Article
  18. Review
  19. Review
  20. The role of alternative splicing in lung cancer.Cancer chemotherapy and pharmacology · 2023
    Review
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 5 institutions in 2 countries.

Andrew T LudlowDepartment of Cell Biology, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX, 75390, USA. atludlow@umich.edu.ORCID http://orcid.org/0000-0003-0423-4800
Mandy Sze WongDepartment of Cell Biology, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX, 75390, USA.
Jerome D RobinDepartment of Cell Biology, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX, 75390, USA.
Kimberly BattenDepartment of Cell Biology, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX, 75390, USA.
Laura YuanDepartment of Cell Biology, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX, 75390, USA.
Tsung-Po LaiDepartment of Cell Biology, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX, 75390, USA.
Nicole DahlsonDepartment of Cell Biology, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX, 75390, USA.
Lu ZhangDepartment of Cell Biology, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX, 75390, USA.
Ilgen MenderDepartment of Cell Biology, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX, 75390, USA.
Enzo TedoneDepartment of Cell Biology, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX, 75390, USA.
Mohammed E SayedDepartment of Cell Biology, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX, 75390, USA.
Woodring E WrightDepartment of Cell Biology, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX, 75390, USA.ORCID http://orcid.org/0000-0001-6838-6665
Jerry W ShayDepartment of Cell Biology, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX, 75390, USA.
Southwestern Medical CenterAix-Marseille Université · FRCold Spring Harbor Laboratory · USUniversity of Michigan · USWashtenaw Community College · US

Funding

UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI GIBBONS, DON LYNN · 1996 to 2024
$57.4M
UT Southwestern Medical Center Simmons Comprehensive Cancer CenterP30CA142543 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI Sandi Leigh Pruitt · 2010 to 2026
$53.7M
Cell Biology Research Improvements and RenovationsC06RR030414 · NCRR · UT SOUTHWESTERN MEDICAL CENTER · PI FITZ, JOHN GREGORY · 2010 to 2010
$15.0M
GENE EXPRESSION IN AGING AND DEVELOPMENTR01AG001228 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI SHAY, JERRY WILLIAM · 1985 to 2018
$7.6M
Cancer Biology Training GrantT32CA124334 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI SHAY, JERRY WILLIAM · 2007 to 2021
$5.3M
Manipulating telomerase alternative splicing for cancer therapyR01CA154805 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI WRIGHT, WOODRING ERIK · 2011 to 2015
$1.6M
Manipulating hTERT splicing in lung cancer cells.R00CA197672 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUDLOW, ANDREW TODD · 2017 to 2019
$738k
Manipulating hTERT splicing in lung cancer cells.K99CA197672 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI LUDLOW, ANDREW TODD · 2016 to 2017
$289k
NCI NIH HHS K99 CA197672NCI NIH HHS P30 CA142543NCI NIH HHS P50 CA070907NCI NIH HHS R00 CA197672NCI NIH HHS R01 CA154805NCI NIH HHS T32 CA124334NCRR NIH HHS C06 RR030414NIA NIH HHS R01 AG001228
6 · The paper itself

Abstract

Alternative splicing is dysregulated in cancer and the reactivation of telomerase involves the splicing of TERT transcripts to produce full-length (FL) TERT. Knowledge about the splicing factors that enhance or silence FL hTERT is lacking. We identified splicing factors that reduced telomerase activity and shortened telomeres using a siRNA minigene reporter screen and a lung cancer cell bioinformatics approach. A lead candidate, NOVA1, when knocked down resulted in a shift in hTERT splicing to non-catalytic isoforms, reduced telomerase activity, and progressive telomere shortening. NOVA1 knockdown also significantly altered cancer cell growth in vitro and in xenografts. Genome engineering experiments reveal that NOVA1 promotes the inclusion of exons in the reverse transcriptase domain of hTERT resulting in the production of FL hTERT transcripts. Utilizing hTERT splicing as a model splicing event in cancer may provide new insights into potentially targetable dysregulated splicing factors in cancer.

Indexed as

Alternative SplicingAnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorComputational BiologyGene DeletionGene SilencingGenetic EngineeringGenome, HumanHeLa CellsHumansLung NeoplasmsMiceMutationNeoplasm TransplantationNeuro-Oncological Ventral AntigenNeuro-Oncological Ventral AntigenNOVA1 protein, humanNova1 protein, mouseRNA-Binding ProteinsRNA, Small InterferingTelomeraseTERT protein, humanTert protein, mouse

Identifiers

PMID30082712
PMCPMC6079032
OpenAlexW2886067672

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.