Evidence map›Paper›PMID 34799689›Full record

ArticleCommunications biology2021

piR-39980 mediates doxorubicin resistance in fibrosarcoma by regulating drug accumulation and DNA repair.

Basudeb Das, Neha Jain, Bibekanand Mallick

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
6.4field-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

21 citing papers in PubMed, 40 citations in OpenAlex.

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  15. Targeting epigenetic regulators to overcome drug resistance in cancers.Signal transduction and targeted therapy · 2023
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  17. In Silico Study of piRNA Interactions with the SARS-CoV-2 Genome.International journal of molecular sciences · 2022
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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

3 authors at 1 institution in 1 country.

Basudeb DasRNAi and Functional Genomics Lab, Department of Life Science, National Institute of Technology Rourkela, Rourkela, 769008, Odisha, India.ORCID http://orcid.org/0000-0001-8782-4392
Neha JainRNAi and Functional Genomics Lab, Department of Life Science, National Institute of Technology Rourkela, Rourkela, 769008, Odisha, India.
Bibekanand MallickRNAi and Functional Genomics Lab, Department of Life Science, National Institute of Technology Rourkela, Rourkela, 769008, Odisha, India. mallickb@nitrkl.ac.in.ORCID http://orcid.org/0000-0003-4311-0720
National Institute of Technology Rourkela · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Resistance to doxorubicin (DOX) is an obstacle to successful sarcoma treatment and a cause of tumor relapse, with the underlying molecular mechanism still unknown. PIWI-interacting RNAs (piRNAs) have been shown to enhance patient outcomes in cancers. However, there are few or no reports on piRNAs affecting chemotherapy in cancers, including fibrosarcoma. The current study aims to investigate the relationship between piR-39980 and DOX resistance and the underlying mechanisms. We reveal that piR-39980 is less expressed in DOX-resistant HT1080 (HT1080/DOX) fibrosarcoma cells. Our results show that inhibition of piR-39980 in parental HT1080 cells induces DOX resistance by attenuating intracellular DOX accumulation, DOX-induced apoptosis, and anti-proliferative effects. Its overexpression in HT1080/DOX cells, on the other hand, increases DOX sensitivity by promoting intracellular DOX accumulation, DNA damage, and apoptosis. The dual-luciferase reporter assay indicates that piR-39980 negatively regulates RRM2 and CYP1A2 via direct binding to their 3'UTRs. Furthermore, overexpressing RRM2 induces DOX resistance of HT1080 cells by rescuing DOX-induced DNA damage by promoting DNA repair, whereas CYP1A2 confers resistance by decreasing intracellular DOX accumulation, which piR-39980 restores. This study reveals that piR-39980 could reduce fibrosarcoma resistance to DOX by modulating RRM2 and CYP1A2, implying that piRNA can be used in combination with DOX.

Indexed as

Antineoplastic AgentsCell Line, TumorDNA RepairDoxorubicinDrug Resistance, NeoplasmFibrosarcomaHEK293 CellsHumansRNA, Small InterferingAntineoplastic AgentsDoxorubicinRNA, Small Interfering

Identifiers

PMID34799689
PMCPMC8605029
OpenAlexW3214235478

What OpenQuestion holds

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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.