ArticleOncotarget2016
Protein phosphatase Mg2+/Mn2+ dependent 1F promotes smoking-induced breast cancer by inactivating phosphorylated-p53-induced signals.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- The phosphatase PPM1F, a negative regulator of integrin activity, is essential for embryonic development and controls tumor cell invasion.BMC biology · 2025Article
- PPM1F regulates ovarian cancer progression by affecting the dephosphorylation of ITGB1.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Article
- The Distinct Biological Effects of 6-Hydroxy-L-Nicotine in Representative Cancer Cell Lines.Molecules (Basel, Switzerland) · 2024Article
- Exploring neurotransmitters and their receptors for breast cancer prevention and treatment.Theranostics · 2023Review
- Article
- Non-coding RNA-associated competitive endogenous RNA regulatory networks: Novel diagnostic and therapeutic opportunities for hepatocellular carcinoma.Journal of cellular and molecular medicine · 2022Review
- α9-Containing Nicotinic Receptors in Cancer.Frontiers in cellular neuroscience · 2021Review
- Nicotinic-nAChR signaling mediates drug resistance in lung cancer.Journal of Cancer · 2020Review
- Article
- CircSLC3A2 functions as an oncogenic factor in hepatocellular carcinoma by sponging miR-490-3p and regulating PPM1F expression.Molecular cancer · 2018Article
- Loss of PPM1F expression predicts tumour recurrence and is negatively regulated by miR-590-3p in gastric cancer.Cell proliferation · 2018Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously demonstrated that the activation of α9-nicotinic acetylcholine receptor (α9-nAchR) signaling by smoking promotes breast cancer formation. To investigate the downstream signaling molecules involved in α9-nAChR-induced breast tumorigenesis, we used real-time polymerase chain reactions and Western blotting to assess expression of protein phosphatase Mg2+/Mn2+ dependent 1F (PPM1F), a Ser/Thr protein phosphatase, in human breast cancer samples (n=167). Additionally, stable PPM1F-knockdown and -overexpressing cell lines were established to evaluate the function of PPM1F. The phosphatase activity of PPM1F in nicotine-treated cells was assessed through Western blotting, confocal microscopy, and fluorescence resonance energy transfer. Higher levels of PPM1F were detected in the breast cancer tissues of heavy smokers (n=7, 12.8-fold) greater than of non-smokers (n= 28, 6.3-fold) (**p=0.01). In vitro, nicotine induced PPM1F expression, whereas α9-nAChR knockdown reduced the protein expression of PPM1F. A series of biochemical experiments using nicotine-treated cells suggested that the dephosphorylation of p53 (Ser-20) and BAX (Ser-184) by PPM1F is a critical posttranslational modification, as observed in breast cancer patients who were heavy smokers. These observations indicate that PPM1F may be a mediator downstream of α9-nAChR that activates smoking-induced carcinogenic signals. Thus, PPM1F expression could be used for prognostic diagnosis or inhibited for cancer prevention and therapy.
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