Evidence map›Paper›PMID 33013387›Full record

ArticleFrontiers in pharmacology2020

PKM2-c-Myc-Survivin Cascade Regulates the Cell Proliferation, Migration, and Tamoxifen Resistance in Breast Cancer.

Pian Yu, Ao-Xue Li, Xi-Sha Chen, Min Tian, Hai-Yan Wang, Xin-Luan Wang, Yi Zhang, Kuan-Song Wang, Yan Cheng

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 45 citations in OpenAlex.

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  17. Phytochemicals Target Multiple Metabolic Pathways in Cancer.Antioxidants (Basel, Switzerland) · 2023
    Review
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  20. Review
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

9 authors at 5 institutions in 1 country.

Pian YuDepartment of Pharmacy, The Second Xiangya Hospital, Central South University, Changsha, China.
Ao-Xue LiDepartment of Pharmacy, The Second Xiangya Hospital, Central South University, Changsha, China.
Xi-Sha ChenDepartment of Pharmacy, The Second Xiangya Hospital, Central South University, Changsha, China.
Min TianDepartment of Pharmacy, The Second Xiangya Hospital, Central South University, Changsha, China.
Hai-Yan WangXiangya School of Pharmaceutical Sciences, Central South University, Changsha, China.
Xin-Luan WangTranslational Medicine R&D Center, Institute of Biomedical and Health Engineering, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.
Yi ZhangDepartment of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Kuan-Song WangDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, China.
Yan ChengDepartment of Pharmacy, The Second Xiangya Hospital, Central South University, Changsha, China.
Central South University · CNSecond Xiangya Hospital of Central South University · CNShenzhen Institutes of Advanced Technology · CNSoochow University · CNXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The M2 isoform of pyruvate kinase (PKM2), as a key glycolytic enzyme, plays important roles in tumorigenesis and chemotherapeutic drug resistance. However, the intricate mechanism of PKM2 as a protein kinase regulating breast cancer progression and tamoxifen resistance needs to be further clarified. Here, we reported that PKM2 controls the expression of survivin by phosphorylating c-Myc at Ser-62. Functionally, PKM2 knockdown suppressed breast cancer cell proliferation and migration, which could be rescued by overexpression of survivin. Interestingly, we found that the level of PKM2 expression was upregulated in the tamoxifen resistant breast cancer cells MCF-7/TAMR, and knockdown of PKM2 sensitized the cells to 4-hydroxytamoxifen (4OH-T). In addition, the elevated level of PKM2 correlates with poor relapse-free survival in breast cancer patients treated with tamoxifen. Overall, our findings demonstrated that PKM2-c-Myc-survivin cascade regulated the proliferation, migration and tamoxifen resistance of breast cancer cells, suggesting that PKM2 represents a novel prognostic marker and an attractive target for breast cancer therapeutics, and that PKM2 inhibitor combined with tamoxifen may be a promising strategy to reverse tamoxifen resistance in breast cancer patients.

Indexed as

breast cancer cellsc-MycM2 isoform of pyruvate kinasesurvivintamoxifen resistance

Identifiers

PMID33013387
PMCPMC7506054
OpenAlexW3083999683

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.