ReviewMolecules (Basel, Switzerland)2017
PP2A as the Main Node of Therapeutic Strategies and Resistance Reversal in Triple-Negative Breast Cancer.
Review in Molecules (Basel, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 20 citations in OpenAlex.
- Yi-qi-hua-yu-jie-du Decoction Inhibits Gastric Cancer Progression by Inducing Tumor-Associated Macrophage Polarization via Modulating PP2A Enzyme Activity to Mediate the PI3K/AKT/NF-κB Axis.Journal of inflammation research · 2026Article
- Ancestral origins are associated with SARS-CoV-2 susceptibility and protection in a Florida patient population.PloS one · 2023Article
- Glutathione Programmed Mitochondria Targeted Delivery of Lonidamine for Effective Against Triple Negative Breast Cancer.International journal of nanomedicine · 2023Article
- Article
- PPP2R2B downregulation is associated with immune evasion and predicts poor clinical outcomes in triple-negative breast cancer.Cancer cell international · 2021Article
- New Cytotoxic Cerebrosides from the Red Sea CucumberMarine drugs · 2020Article
- 2'-Hydroxyflavanone induced changes in the proteomic profile of breast cancer cells.Journal of proteomics · 2019Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple negative breast cancer (TNBC), is defined as a type of tumor lacking the expression of estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2). The ER, PR and HER2 are usually the molecular therapeutic targets for breast cancers, but they are ineffective for TNBC because of their negative expressions, so chemotherapy is currently the main treatment strategy in TNBC. However, drug resistance remains a major impediment to TNBC chemotherapeutic treatment. Recently, the protein phosphatase 2A (PP2A) has been found to regulate the phosphorylation of some substrates involved in the relevant target of TNBC, such as cell cycle control, DNA damage responses, epidermal growth factor receptor, immune modulation and cell death resistance, which may be the effective therapeutic strategies or influence drug sensitivity to TNBCs. Furthermore, PP2A has also been found that could induce ER re-expression in ER-negative breast cancer cells, and which suggests PP2A could promote the sensitivity of tamoxifen to TNBCs as a resistance reversal agent. In this review, we will summarize the potential therapeutic value of PP2A as the main node in developing targeting agents, disrupting resistance or restoring drug sensitivity in TNBC.
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Registered trials
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.