ArticleOncotarget2015
Elevated MARCKS phosphorylation contributes to unresponsiveness of breast cancer to paclitaxel treatment.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- MARCKS contributes to stromal cancer-associated fibroblast activation and facilitates ovarian cancer metastasis.Oncotarget · 2016Pooled it
- A peptide against the N-terminus of myristoylated alanine-rich C kinase substrate promotes neuronal differentiation in SH-SY5Y human neuroblastoma cells.The Journal of veterinary medical science · 2024Article
- Integrated analysis identifies microRNA-188-5p as a suppressor of AKT/mTOR pathway in renal cancer.Cancer science · 2023Article
- Review
- Article
- The Profile of MicroRNA Expression and Potential Role in the Regulation of Drug-Resistant Genes in Doxorubicin and Topotecan Resistant Ovarian Cancer Cell Lines.International journal of molecular sciences · 2022Article
- Transcriptome Analysis of Liver Cancer Cell Huh-7 Treated With Metformin.Frontiers in pharmacology · 2022Article
- The myristoylated alanine-rich C-kinase substrates (MARCKS): A membrane-anchored mediator of the cell function.Autoimmunity reviews · 2021Review
- Pharmacological rescue of cognitive function in a mouse model of chemobrain.Molecular neurodegeneration · 2021Article
- Pathophysiological roles of myristoylated alanine-rich C-kinase substrate (MARCKS) in hematological malignancies.Biomarker research · 2021Review
- Therapeutic targeting of argininosuccinate synthase 1 (ASS1)-deficient pulmonary fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Restoration of MARCKS enhances chemosensitivity in cancer.Journal of cancer research and clinical oncology · 2020Article
- Tackling MARCKS-PIP3 circuit attenuates fibroblast activation and fibrosis progression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Myristoylated alanine-rich C-kinase substrate effector domain phosphorylation regulates the growth and radiation sensitization of glioblastoma.International journal of oncology · 2019Article
- Targeting the phosphorylation site of myristoylated alanine-rich C kinase substrate alleviates symptoms in a murine model of steroid-resistant asthma.British journal of pharmacology · 2019Article
- Prognostic Value of Upregulation of Myristoylated Alanine-Rich C-Kinase Substrate in Gastric Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- MARCKS protein overexpression is associated with poor prognosis in male breast cancer.Cancer biomarkers : section A of Disease markers · 2019Article
- MARCKS and Lung Disease.American journal of respiratory cell and molecular biology · 2019Review
- Epigenetic silencing of tumor suppressor Par-4 promotes chemoresistance in recurrent breast cancer.The Journal of clinical investigation · 2018Article
- Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Accumulating evidence has suggested that myristoylated alanine-rich C-kinase substrate (MARCKS) is critical for regulating multiple pathophysiological processes. However, the molecular mechanism underlying increased phosphorylation of MARCKS at Ser159/163 (phospho-MARCKS) and its functional consequence in neoplastic disease remain to be established. Herein, we investigated how phospho-MARCKS is regulated in breast carcinoma, and its role in the context of chemotherapy. In a screen of patients with breast tumors, we find that the abundance of phospho-MARCKS, not MARCKS protein per se, increased in breast cancers and positively correlated with tumor grade and metastatic status. Among chemotherapeutic agents, mitotic inhibitors, including paclitaxel, vincristine or eribulin, notably promoted phospho-MARCKS accumulation in multiple breast cancer cells. We further show that phospho-MARCKS acted upstream of Src activation upon paclitaxel exposure. Reduction of phospho-MARCKS by knockdown of MARCKS or pharmacological agents increased paclitaxel sensitivity. Particularly, a known phospho-MARCKS inhibitor, MANS peptide, was demonstrated to increase paclitaxel efficacy and attenuate angiogenesis/metastasis of xenografted breast cancer cells by decreasing abundance of phospho-MARCKS and messages of inflammatory mediators. Our data suggest that unresponsiveness of breast cancer to paclitaxel treatment is, at least in part, mediated by phospho-MARCKS and also provide an alternative therapeutic strategy against breast cancer by improving taxanes sensitivity.
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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.