Combined Fascin-1 and MAP17 Expression in Breast Cancer Identifies Patients with High Risk for Disease Recurrence

Tampaki, Ekaterini Christina; Tampakis, Athanasios; Nonni, Afroditi; Flüe, Markus von; Patsouris, Efstratios; Kontzoglou, Konstantinos; Kouraklis, Gregory

doi:10.1007/s40291-019-00411-3

Cited by 13 publications

(6 citation statements)

References 53 publications

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“…Specifically, the high expression of MAP17 was associated with excessive proliferation and reduced apoptosis in PTC cells, as well as tumor growth. Consistently, the carcinogenic effects of MAP17 have also been demonstrated in non-small cell lung cancer and breast cancer [26,27]. Collectively, it suggested that MAP17 may serve as a potential prognostic marker for PTC.…”

Section: Discussionsupporting

confidence: 53%

80MAP17 promotes the tumorigenesis of papillary thyroid carcinoma by reducing the stability of p53

Yu¹,

Lü²,

Chen

et al. 2021

Front Biosci (Landmark Ed)

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Section: Discussionsupporting

confidence: 53%

80MAP17 promotes the tumorigenesis of papillary thyroid carcinoma by reducing the stability of p53

Yu¹,

Lü²,

Chen

et al. 2021

Front Biosci (Landmark Ed)

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“…In addition, we observed how MAP17 levels increase in cancer cells during tumor progression, being higher in metastatic samples than in primary tumor samples, suggesting that this protein could have an important role in progression from primary to metastatic tumors, where this protein usually has higher expression levels 1 , 8 , 12 , 13 . In fact, in breast cancer, MAP17 expression has been correlated with a high risk of disease recurrence 50 . The observed increase in MAP17 expression can be due to progressive MAP17 gene demethylation 1 , 2 , 8 , increasing its expression in some of the primary tumor cells.…”

Section: Discussionmentioning

confidence: 99%

Breast tumor cells promotes the horizontal propagation of EMT, stemness, and metastasis by transferring the MAP17 protein between subsets of neoplastic cells

et al. 2020

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MAP17 (PDZK1IP1) is a small protein regulating inflammation and tumor progression, upregulated in a broad range of carcinomas. MAP17 levels increase during tumor progression in a large percentage of advanced tumors. In the present work, we explored the role of this protein shaping tumor evolution. Here we show that in breast cancer, cells increased MAP17 levels in tumors by demethylation induced multiple changes in gene expression through specific miRNAs downregulation. These miRNA changes are dependent on Notch pathway activation. As a consequence, epithelial mesenchymal transition (EMT) and stemness are induced promoting the metastatic potential of these cells both in vitro and in vivo. Furthermore, MAP17 increased the exosomes in tumor cells, where MAP17 was released as cargo, and this horizontal propagation also increased the EMT in the recipient cells. Importantly, an antibody against MAP17 in the media reduces the EMT and stemness alterations promoted by the conditioned media from MAP17-expressing cells. Therefore, MAP17 expression promotes the horizontal propagation of EMT and metastasis by transferring the MAP17 protein between subsets of neoplastic cells. Thus, MAP17 can be used to describe a new mechanism for cell malignity at distance, without the involvement of genetic or epigenetic modifications. MAP17 can also be taken in consideration as new target for metastatic high-grade breast tumors.

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“…Tumor neovascularization is an important factor for tumor cell growth, invasion and metastasis, and the main factor for tumor neovascularization is VEGF, so the key to tumor antiangiogenesis is the treatment of VEGF, which can be used as an important strategy for targeted treatment of breast cancer [19]. Endocrine therapy is one of the main means of systemic therapy for breast cancer (as shown in Figure 2).…”

Section: Endocrine Targeted Therapymentioning

confidence: 99%

Research on Cellular Immune Targeted Drug Therapy for Breast Cancer based on Bioinformatics

Meng¹

2023

IJBLS

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Targeted therapy, because of its precise location, high efficiency and low toxicity, has become an important tumor treatment method besides traditional treatments such as surgery, radiotherapy and chemotherapy. Targeted drugs can deliver therapeutic drugs to target organs to the maximum extent, but have little effect on non-target organs, thus achieving high-efficiency and low-toxicity therapeutic effects, especially for treating diseases such as cancer. At the cellular and molecular level, molecular targeting means that drugs enter the body and specifically bind with carcinogenic sites on tumor cells, resulting in the death of tumor cells, but it does not affect the surrounding normal tissues and cells. Studying the pathogenesis and related genes of breast cancer plays an active role in the early diagnosis and treatment of breast cancer, and effectively relieves the current status of clinical breast cancer treatment. In-depth study on molecular typing of breast cancer can provide further reference for the selection of clinical treatment schemes more effectively. This paper discusses the cellular immune targeted drug therapy for breast cancer from the perspective of bioinformatics.

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Combined Fascin-1 and MAP17 Expression in Breast Cancer Identifies Patients with High Risk for Disease Recurrence

Cited by 13 publications

References 53 publications

80MAP17 promotes the tumorigenesis of papillary thyroid carcinoma by reducing the stability of p53

80MAP17 promotes the tumorigenesis of papillary thyroid carcinoma by reducing the stability of p53

Breast tumor cells promotes the horizontal propagation of EMT, stemness, and metastasis by transferring the MAP17 protein between subsets of neoplastic cells

Research on Cellular Immune Targeted Drug Therapy for Breast Cancer based on Bioinformatics

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