Evidence map›Paper›PMID 32011210›Full record

ArticleCell cycle (Georgetown, Tex.)2020

Targeting PP2A inhibits the growth of triple-negative breast cancer cells.

Mohammed Hafiz Uddin, Julio M Pimentel, Madhumita Chatterjee, Joshu E Allen, Zhengping Zhuang, Gen Sheng Wu

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. The Benthic DinoflagellateMarine drugs · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Targeting PP2A for cancer therapeutic modulation.Cancer biology & medicine · 2022
    Review
  9. Article
  10. 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

6 authors at 3 institutions in 1 country.

Mohammed Hafiz UddinDepartment of Oncology and Pathology, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI, USA.
Julio M PimentelDepartment of Oncology and Pathology, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI, USA.
Madhumita ChatterjeeDepartment of Oncology and Pathology, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI, USA.
Joshu E AllenDepartment of Research and Development, Oncoceutics, Inc, Philadelphia, PA, USA.
Zhengping ZhuangNeuro-Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Gen Sheng WuDepartment of Oncology and Pathology, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI, USA.
Wayne State University · USCenter for Cancer Research · USOncoceutics (United States) · US

Funding

Developing targeted therapies for triple-negative breast cancerR01CA174949 · NCI · WAYNE STATE UNIVERSITY · PI WU, GEN SHENG · 2014 to 2020
$1.4M
NCI NIH HHS R01 CA174949
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) does not respond to widely used targeted/endocrine therapies because of the absence of progesterone and estrogen receptors and HER2 amplification. It has been shown that the majority of TNBC cells are highly sensitive to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis, but the development of TRAIL resistance limits its efficacy. We previously found that protein phosphatase 2A (PP2A) plays an important role in TRAIL resistance. In this study, we evaluated the effects of PP2A inhibition on cell death in TRAIL-resistant TNBC cells. We found that the PP2A inhibitor LB-100 effectively inhibits the growth of a panel of TNBC cell lines including lines that are intrinsically resistant to TRAIL. Using two TRAIL-resistant cell lines generated from TRAIL-sensitive parental cells (MDA231 and SUM159), we found that both TRAIL-sensitive and -resistant cell lines are equally sensitive to LB-100. We also found that LB-100 sensitizes TNBC cells to clinically used chemotherapeutical agents, including paclitaxel and cisplatin. Importantly, we found that LB-100 effectively inhibits the growth of MDA468 tumors in mice in vivo without apparent toxicity. Collectively, these data suggest that pharmacological inhibition of PP2A activity could be a novel therapeutic strategy for treating patients with TNBC in a clinical setting.

Indexed as

AnimalsApoptosisCell Line, TumorCisplatinDrug Resistance, NeoplasmDrug SynergismFemaleHumansMicePiperazinesProtein Phosphatase 2TNF-Related Apoptosis-Inducing LigandTriple Negative Breast NeoplasmsCisplatinLB100PiperazinesProtein Phosphatase 2TNF-Related Apoptosis-Inducing LigandapoptosisPP2A inhibitorTNBCTRAIL

Identifiers

PMID32011210
PMCPMC7100985
OpenAlexW3004576606

What OpenQuestion holds

Textmetadata
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.