Evidence map›Paper›PMID 34359939›Full record

ArticleCells2021

CK2α/CSNK2A1 Induces Resistance to Doxorubicin through SIRT6-Mediated Activation of the DNA Damage Repair Pathway.

Usama Khamis Hussein, Asmaa Gamal Ahmed, Yiping Song, Kyoung Min Kim, Young Jae Moon, Ae-Ri Ahn, Ho Sung Park, Su Jin Ahn, See-Hyoung Park, Jung Ryul Kim and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Ellagic Acid Mediates the Delay of Dermal Fibroblast Senescence via CSNK2A1.Clinical, cosmetic and investigational dermatology · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. 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

11 authors at 4 institutions in 2 countries.

Usama Khamis HusseinDepartment of Pathology, Jeonbuk National University Medical School, Jeonju 54896, Korea.
Asmaa Gamal AhmedDepartment of Pathology, Jeonbuk National University Medical School, Jeonju 54896, Korea.
Yiping SongDepartment of Orthopedic Surgery, Jeonbuk National University Medical School, Jeonju 54896, Korea.
Kyoung Min KimDepartment of Pathology, Jeonbuk National University Medical School, Jeonju 54896, Korea.
Young Jae MoonResearch Institute of Clinical Medicine of Jeonbuk National University-Biomedical Research Institute of Jeonbuk National University Hospital, Jeonju 54907, Korea.ORCID 0000-0002-5285-7618
Ae-Ri AhnDepartment of Pathology, Jeonbuk National University Medical School, Jeonju 54896, Korea.
Ho Sung ParkDepartment of Pathology, Jeonbuk National University Medical School, Jeonju 54896, Korea.ORCID 0000-0002-4879-874X
Su Jin AhnDepartment of Biochemistry and Molecular Biology, Jeonbuk National University Medical School, Jeonju 54896, Korea.
See-Hyoung ParkDepartment of Bio and Chemical Engineering, Hongik University, Sejong 30016, Korea.ORCID 0000-0003-0020-7389
Jung Ryul KimResearch Institute of Clinical Medicine of Jeonbuk National University-Biomedical Research Institute of Jeonbuk National University Hospital, Jeonju 54907, Korea.
Kyu Yun JangDepartment of Pathology, Jeonbuk National University Medical School, Jeonju 54896, Korea.ORCID 0000-0002-5276-4446
Jeonbuk National University Hospital · KRBeni-Suef University · EGJeonbuk National University · KRHongik University · KR

Funding

National Research Foundation of Korea 2017R1A5A2015061National Research Foundation of Korea 2017R1E1A1A01074533
6 · The paper itself

Abstract

CK2α/CSNK2A1 is involved in cancer progression by phosphorylating various signaling molecules. Considering the role of CSNK2A1 in cancer progression and the phosphorylation of SIRT6 and the role of SIRT6 in chemoresistance through the DNA damage repair pathway, CSNK2A1 and SIRT6 might be involved in resistance to conventional anti-cancer therapies. We evaluated the expression of CSNK2A1 and phosphorylated SIRT6 in the 37 osteosarcoma patients and investigated the effects of CSNK2A1 and the phosphorylation of SIRT6 on Ser338 on resistance to the anti-cancer effects of doxorubicin. Higher expression of CSNK2A1 and phosphorylated SIRT6 was associated with shorter survival in osteosarcoma patients. U2OS and KHOS/NP osteosarcoma cells with induced overexpression of CSNK2A1 were resistant to the cytotoxic effects of doxorubicin, and the knock-down of CSNK2A1 potentiated the cytotoxic effects of doxorubicin. CSNK2A1 overexpression-mediated resistance to doxorubicin was associated with SIRT6 phosphorylation and the induction of the DNA damage repair pathway molecules. CSNK2A1- and SIRT6-mediated resistance to doxorubicin in vivo was attenuated via mutation of SIRT6 at the Ser338 phosphorylation site. Emodin, a CSNK2A1 inhibitor, potentiated the cytotoxic effects of doxorubicin in osteosarcoma cells. This study suggests that blocking the CSNK2A1-SIRT6-DNA damage repair pathway might be a new therapeutic stratagem for osteosarcomas.

Indexed as

DNA DamageDNA RepairDrug Resistance, NeoplasmAdultApoptosisCasein Kinase IICell Line, TumorCell ProliferationDoxorubicinEmodinFemaleHumansKaplan-Meier EstimateMaleMultivariate AnalysisPhosphorylationCasein Kinase IICSNK2A1 protein, humanDoxorubicinEmodinSIRT6 protein, humanSirtuinsCSNK2A1DNA damagedoxorubicinosteosarcomaprognosisSIRT6

Identifiers

PMID34359939
PMCPMC8303481
OpenAlexW3174616711

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.