Evidence map›Paper›PMID 26172393›Full record

ArticleOncotarget2015

Phosphorylation of apoptosis repressor with caspase recruitment domain by protein kinase CK2 contributes to chemotherapy resistance by inhibiting doxorubicin induced apoptosis.

Jianxun Wang, Chang Feng, Yuqi He, Wei Ding, Jianqiu Sheng, Muhammad Arshad, Xiaojie Zhang, Peifeng Li

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

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  11. Role of protein kinase CK2 in antitumor drug resistance.Journal of experimental & clinical cancer research : CR · 2019
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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

8 authors at 4 institutions in 1 country.

Jianxun WangInstitute for Translational Medicine, Medical College of Qingdao University, Qingdao, 266021, China.
Chang FengNational Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
Yuqi HeDepartment of Gastroenterology, Beijing Military General Hospital, Beijing, 100700, China.
Wei DingAffiliated Hospital, Medical College of Qingdao University, Qingdao, 266003, China.
Jianqiu ShengDepartment of Gastroenterology, Beijing Military General Hospital, Beijing, 100700, China.
Muhammad ArshadNational Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
Xiaojie ZhangNational Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
Peifeng LiInstitute for Translational Medicine, Medical College of Qingdao University, Qingdao, 266021, China.
Qingdao University · CNChinese Academy of Sciences · CNThe Military General Hospital of Beijing PLA · CNInstitute of Zoology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of cancer resistance to chemotherapy is the major obstacle to cancer therapy. Here, we identified that the phosphorylation of apoptosis repressor with caspase recruitment domain (ARC) at threonine 149 was essential to inhibit doxorubicin (DOX) induced apoptosis and mitochondrial fission in cancer cells. Our further study showed that casein kinase II (CK2) inhibitors could decrease the phosphorylation levels of ARC and make cancer cells sensitive to undergoing apoptosis. Furthermore, CK2α and CK2α', catalytic subunits of CK2, were observed to translocate into nuclear in cancer cells with the treatment of DOX. Finally, the synergistically therapeutic effect by combining DOX and CK2 inhibitor was confirmed in tumor xenograft model. Taken together, our results revealed that CK2-mediated phosphorylation of ARC contributed to chemotherapy resistance by inhibiting DOX induced apoptosis and combining DOX with CK2 inhibitor could induce apoptosis of cancer cells synergistically by down-regulating the phosphorylation of ARC. Therefore, development of new therapeutic strategies based on ARC and CK2, is promising for overcoming cancer resistance to chemotherapy.

Indexed as

ApoptosisDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticAnimalsAntineoplastic AgentsCasein Kinase IICaspasesCell Line, TumorCell NucleusCell SurvivalCytoskeletal ProteinsDoxorubicinFemaleHeLa CellsHumansMiceactivity regulated cytoskeletal-associated proteinAntineoplastic AgentsCasein Kinase IICaspasesCSNK2A1 protein, humanCytoskeletal ProteinsDoxorubicinNerve Tissue ProteinsapoptosisARCchemotherapy resistanceCK2doxorubicin

Identifiers

PMID26172393
PMCPMC4695019
OpenAlexW1866397392

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.