Evidence map›Paper›PMID 33028635›Full record

ArticleThe Journal of biological chemistry2020

Dysregulation of hsa-miR-34a and hsa-miR-449a leads to overexpression of PACS-1 and loss of DNA damage response (DDR) in cervical cancer.

Mysore S Veena, Santanu Raychaudhuri, Saroj K Basak, Natarajan Venkatesan, Parameet Kumar, Roopa Biswas, Rita Chakrabarti, Jing Lu, Trent Su, Marcus Gallagher-Jones and 9 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Oncology research · 2026
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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

19 authors at 7 institutions in 1 country.

Mysore S VeenaDepartment of Surgery, VAGLAHS West Los Angeles and David Geffen School of Medicine at UCLA, Los Angeles, California, USA.
Santanu RaychaudhuriDepartment of Microbiology, Immunology and Molecular Genetics, David Geffen School of Medicine at UCLA, Los Angeles, California, USA.
Saroj K BasakDepartment of Surgery, VAGLAHS West Los Angeles and David Geffen School of Medicine at UCLA, Los Angeles, California, USA; Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, USA.
Natarajan VenkatesanDepartment of Surgery, VAGLAHS West Los Angeles and David Geffen School of Medicine at UCLA, Los Angeles, California, USA.
Parameet KumarDepartment of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences, Bethesda, Maryland, USA.
Roopa BiswasDepartment of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences, Bethesda, Maryland, USA.
Rita ChakrabartiDepartment of Surgery, VAGLAHS West Los Angeles and David Geffen School of Medicine at UCLA, Los Angeles, California, USA.
Jing LuDepartment of Molecular, Cell, and Developmental Biology, UCLA, Los Angeles, California, USA.
Trent SuInstitute for Quantitative and Computational Biology and Department of Biological Chemistry, UCLA, Los Angeles, California, USA.
Marcus Gallagher-JonesDepartment of Chemistry and Biochemistry, UCLA, Los Angeles, California, USA.
Marco MorselliDepartment of Molecular, Cell, and Developmental Biology, UCLA, Los Angeles, California, USA.
Haiqing FuDevelopmental Therapeutics Branch, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland, USA.
Matteo PellegriniDepartment of Molecular, Cell, and Developmental Biology, UCLA, Los Angeles, California, USA.
Theodore GoldsteinInstitute of Computational Sciences, University of California San Francisco, San Francisco, California, USA.
Mirit I AladjemDevelopmental Therapeutics Branch, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland, USA.
Matthew B RettigDepartment of Medicine, VAGLAHS/David Geffen School of Medicine at UCLA, Los Angeles, California, USA.
Sharon P WilczynskiDepartment of Pathology, City of Hope Medical Center, Duarte, California, USA.
Daniel Sanghoon ShinDepartment of Medicine, VAGLAHS/David Geffen School of Medicine at UCLA, Los Angeles, California, USA.
Eri S SrivatsanDepartment of Surgery, VAGLAHS West Los Angeles and David Geffen School of Medicine at UCLA, Los Angeles, California, USA. Electronic address: esrivats@g.ucla.edu.
University of California, Los Angeles · USVA West Los Angeles Medical Center · USNational Institutes of Health · USUniformed Services University of the Health Sciences · USCity Of Hope National Medical Center · USQB3 · USUniversity of California, San Francisco · US

Funding

Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Samuel Wheeler French · 1985 to 2026
$134.5M
Virology CoreP30AI028697 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KITCHEN, SCOTT G · 1991 to 2018
$39.9M
Stanford and Northrop Grumman proposal for the Oncology Models ForumU24CA195858 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BUTTE, ATUL J · 2015 to 2019
$4.7M
NCI NIH HHS P30 CA016042NCI NIH HHS U24 CA195858NIAID NIH HHS P30 AI028697
6 · The paper itself

Abstract

We have observed overexpression of PACS-1, a cytosolic sorting protein in primary cervical tumors. Absence of exonic mutations and overexpression at the RNA level suggested a transcriptional and/or posttranscriptional regulation. University of California Santa Cruz genome browser analysis of PACS-1 micro RNAs (miR), revealed two 8-base target sequences at the 3' terminus for hsa-miR-34a and hsa-miR-449a. Quantitative RT-PCR and Northern blotting studies showed reduced or loss of expression of the two microRNAs in cervical cancer cell lines and primary tumors, indicating dysregulation of these two microRNAs in cervical cancer. Loss of PACS-1 with siRNA or exogenous expression of hsa-miR-34a or hsa-miR-449a in HeLa and SiHa cervical cancer cell lines resulted in DNA damage response, S-phase cell cycle arrest, and reduction in cell growth. Furthermore, the siRNA studies showed that loss of PACS-1 expression was accompanied by increased nuclear γH2AX expression, Lys

Indexed as

DNA DamageDrug Resistance, NeoplasmFemaleG1 PhaseHeLa CellsHumansMicroRNAsRNA, NeoplasmS Phase Cell Cycle CheckpointsTumor Suppressor Protein p53Uterine Cervical NeoplasmsVesicular Transport ProteinsMicroRNAsMIRN34 microRNA, humanMIRN449 microRNA, humanPACS1 protein, humanRNA, NeoplasmTP53 protein, humanTumor Suppressor Protein p53Vesicular Transport Proteinscancer biologycervical cancerDNA damage responsegenome stabilityhsa-miR-449ahsa-miRNA-34anuclear translocationnuclear transportoncogenep53 acetylationPACS-1trafficking proteintumortumor suppressor gene

Identifiers

PMID33028635
PMCPMC7863911
OpenAlexW3092511915

What OpenQuestion holds

Textmetadata
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.