Evidence map›Paper›PMID 29976159›Full record

ArticleBMC cancer2018

MASTL inhibition promotes mitotic catastrophe through PP2A activation to inhibit cancer growth and radioresistance in breast cancer cells.

Yi Na Yoon, Min Ho Choe, Kwan-Young Jung, Sang-Gu Hwang, Jeong Su Oh, Jae-Sung Kim

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

32 citing papers in PubMed, 40 citations in OpenAlex.

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  10. IL-22 regulates MASTL expression in intestinal epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2024
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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

6 authors at 5 institutions in 1 country.

Yi Na YoonDivision of Radiation Cancer Research, Korea Institute of Radiological and Medical Sciences, 215-4 Gongneung-Dong, Nowon-Ku, Seoul, 139-706, South Korea.
Min Ho ChoeDivision of Radiation Cancer Research, Korea Institute of Radiological and Medical Sciences, 215-4 Gongneung-Dong, Nowon-Ku, Seoul, 139-706, South Korea.
Kwan-Young JungCenter for Medicinal Chemistry, Korea Research Institute of Chemical Technology, Daejeon, South Korea.
Sang-Gu HwangDivision of Radiation Cancer Research, Korea Institute of Radiological and Medical Sciences, 215-4 Gongneung-Dong, Nowon-Ku, Seoul, 139-706, South Korea.
Jeong Su OhDepartment of Integrative Biotechnology, Sungkyunkwan University, Suwon, South Korea. ohjs@skku.edu.
Jae-Sung KimDivision of Radiation Cancer Research, Korea Institute of Radiological and Medical Sciences, 215-4 Gongneung-Dong, Nowon-Ku, Seoul, 139-706, South Korea. jaesung@kirams.re.kr.ORCID http://orcid.org/0000-0002-8017-4515
Korea Institute of Radiological and Medical Sciences · KRKorea Research Institute of Chemical Technology · KRKorea University · KRScience and Technology Policy Institute · KRSungkyunkwan University · KR

Funding

2016 SETAC Asia/Pacific ConferenceR13ES027302 · NIEHS · SOCIETY/ENVIRONMENTAL TOXICOLOGY/CHEM · PI MENZIE, CHARLES · 2016 to 2016
$6k
a grant of the Korea Institute of Radiological and Medical Sciences(KIRAMS), funded by Ministry of Science and ICT(MSIT), Republic of Korea 50531-2018NIEHS NIH HHS 27302C0028the National R&D Program for Cancer Control, Ministry of Health and Welfare, Republic of Korea HA17C0028
6 · The paper itself

Abstract

backgroundAlthough MASTL (microtubule-associated serine/threonine kinase-like) is a key mitotic kinase that regulates mitotic progression through the inactivation of tumor suppressor protein phosphatase 2A (PP2A), the antitumor mechanism of MASTL targeting in cancer cells is still unclear.

methodsMASTL expression was evaluated by using breast cancer tissue microarrays and public cancer databases. The effects of MASTL depletion with siRNAs were evaluated in various breast cancer cells or normal cells. Various methods, including cell viability, cell cycle, soft agar, immunoblotting, immunofluorescence, PP2A activity, live image, and sphere forming assay, were used in this study.

resultsThis study showed the oncosuppressive mechanism of MASTL targeting that promotes mitotic catastrophe through PP2A activation selectively in breast cancer cells. MASTL expression was closely associated with tumor progression and poor prognosis in breast cancer. The depletion of MASTL reduced the oncogenic properties of breast cancer cells with high MASTL expression, but did not affect the viability of non-transformed normal cells with low MASTL expression. With regard to the underlying mechanism, we found that MASTL inhibition caused mitotic catastrophe through PP2A activation in breast cancer cells. Furthermore, MASTL depletion enhanced the radiosensitivity of breast cancer cells with increased PP2A activity. Notably, MASTL depletion dramatically reduced the formation of radioresistant breast cancer stem cells in response to irradiation.

conclusionOur data suggested that MASTL inhibition promoted mitotic catastrophe through PP2A activation, which led to the inhibition of cancer cell growth and a reversal of radioresistance in breast cancer cells.

Indexed as

MitosisRadiation ToleranceBreast NeoplasmsCell Cycle ProteinsCell Line, TumorCell ProliferationEnzyme ActivationFemaleHumansMicrotubule-Associated ProteinsNeoplastic Stem CellsPolo-Like Kinase 1PrognosisProtein Phosphatase 2Protein Serine-Threonine KinasesProto-Oncogene ProteinsCell Cycle ProteinsMASTL protein, humanMicrotubule-Associated ProteinsPolo-Like Kinase 1Protein Phosphatase 2Protein Serine-Threonine KinasesProto-Oncogene ProteinsBreast cancerMASTLMitotic catastropheRadiation

Identifiers

PMID29976159
PMCPMC6034325
OpenAlexW2856419391

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.