PI3K-based molecular signatures link high PI3K pathway activity with low ER levels in ER<sup>+</sup>breast cancer

Sánchez, Àlex; Villanueva, Josep

doi:10.1586/epr.10.103

Cited by 5 publications

(5 citation statements)

References 9 publications

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“…Furthermore, the nonreceptor tyrosine kinase focal adhesion kinase (FAK) is associated with highly invasive breast cancers, and it mediates several pathways leading to proliferation, migration, and adhesion [14]. Phosphorylation is required for FAK activation, and it has been shown that estrogens are able to promote rapid phosphorylation of FAK at tyrosines residues [15]. …”

Section: Introductionmentioning

confidence: 99%

The Exposure of Breast Cancer Cells to Fulvestrant and Tamoxifen Modulates Cell Migration Differently

Lymperatou

Giannopoulou

Koutras

et al. 2013

BioMed Research International

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There is no doubt that there are increased benefits of hormonal therapy to breast cancer patients; however, current evidence suggests that estrogen receptor (ER) blockage using antiestrogens is associated with a small induction of invasiveness in vitro. The mechanism by which epithelial tumor cells escape from the primary tumor and colonize to a distant site is not entirely understood. This study investigates the effect of two selective antagonists of the ER, Fulvestrant (Fulv) and Tamoxifen (Tam), on the invasive ability of breast cancer cells. We found that 17β-estradiol (E2) demonstrated a protective role regarding cell migration and invasion. Fulv did not alter this effect while Tam stimulated active cell migration according to an increase in Snail and a decrease in E-cadherin protein expression. Furthermore, both tested agents increased expression of matrix metalloproteinases (MMPs) and enhanced invasive potential of breast cancer cells. These changes were in line with focal adhesion kinase (FAK) rearrangement. Our data indicate that the anti-estrogens counteracted the protective role of E2 concerning migration and invasion since their effect was not limited to antiproliferative events. Although Fulv caused a less aggressive result compared to Tam, the benefits of hormonal therapy concerning invasion and metastasis yet remain to be investigated.

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Section: Introductionmentioning

confidence: 99%

The Exposure of Breast Cancer Cells to Fulvestrant and Tamoxifen Modulates Cell Migration Differently

Lymperatou

Giannopoulou

Koutras

et al. 2013

BioMed Research International

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“…Bacterial infection causes chronic inflammation, which leads to tumor development and progression 14, 16, 27, 29, 30, 33 . Particularly, NF-kB activation plays tumor-promoting role of immune and inflammatory responses 30 .…”

Section: Discussionmentioning

confidence: 99%

“…PAFR is a direct regulator of PI3K/AKT and NF-kB signaling pathways whose hyperactivations paly essential roles in tumor development and progression 14,[26][27][28][29][30] . We therefore evaluated expression of key molecular signatures of the pathways in cancer cells incubated with or without SP.…”

Section: Sp Infection Contributes To Lung Tumorigenesis By Stimulatin...mentioning

confidence: 99%

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Streptococcus Pneumoniae Promotes Lung Tumorigenesis by Activating PI3K/AKT and NF-kB Pathways via Binding PspC to PAFR

Zhou

Holden

et al. 2022

Preprint

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Streptococcus pneumoniae (SP) is associated with lung cancer, yet its role in the tumorigenesis remains uncertain. Herein we find that SP attaches to lung cancer cells via binding pneumococcal surface protein C (PspC) to platelet-activating factor receptor (PAFR), a receptor overexpressed in lung tumors. Interaction between PspC and PAFR stimulates cell proliferation and activates PI3K/AKT and NF-kB signaling pathways, which triggers a pro-inflammatory response. Lung cancer cells infected with SP rapidly form larger tumors in BALB/C mice compared to untreated cells. Mice treated with tobacco carcinogen and SP develop more lung tumors and had shorter survival than mice treated with the carcinogen alone. Mutating PspC or deleting PAFR abolishes the tumor-promoting effects of SP. Overabundance of SP is found in lung tumors of patients with lung cancer and associated with the survival. SP plays a driving role in lung tumorigenesis by activating PI3K/AKT and NF-kB pathways via binding PspC to PAFR and provides a microbial target for diagnosis and treatment of the disease.

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“…Thus, the focus of cancer research has changed from the search for a single cancer biomarker to the understanding of complex oncogenic signaling pathways [13,14].…”

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confidence: 99%

Proteomic Tools for Cancer Research: Updating the Oncoproteomics

Panis

2013

J Proteomics Bioinform

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PI3K-based molecular signatures link high PI3K pathway activity with low ER levels in ER⁺breast cancer

Cited by 5 publications

References 9 publications

The Exposure of Breast Cancer Cells to Fulvestrant and Tamoxifen Modulates Cell Migration Differently

The Exposure of Breast Cancer Cells to Fulvestrant and Tamoxifen Modulates Cell Migration Differently

Streptococcus Pneumoniae Promotes Lung Tumorigenesis by Activating PI3K/AKT and NF-kB Pathways via Binding PspC to PAFR

Proteomic Tools for Cancer Research: Updating the Oncoproteomics

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PI3K-based molecular signatures link high PI3K pathway activity with low ER levels in ER+breast cancer

Cited by 5 publications

References 9 publications

The Exposure of Breast Cancer Cells to Fulvestrant and Tamoxifen Modulates Cell Migration Differently

The Exposure of Breast Cancer Cells to Fulvestrant and Tamoxifen Modulates Cell Migration Differently

Streptococcus Pneumoniae Promotes Lung Tumorigenesis by Activating PI3K/AKT and NF-kB Pathways via Binding PspC to PAFR

Proteomic Tools for Cancer Research: Updating the Oncoproteomics

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PI3K-based molecular signatures link high PI3K pathway activity with low ER levels in ER⁺breast cancer