Filippo Acconcia
Roma Tre University
PalmitoylationReceptorEstrogen receptor alphaKinaseChemistryApoptosisCancer researchBiochemistryMAPK/ERK pathwayCell growthSignal transductionProtein kinase BIntracellularEstrogen receptorTranscription factorPI3K/AKT/mTOR pathwayBiologyCell biologyCancer cellEstrogen receptor beta
65Publications
30H-index
3,057Citations
Publications 68
Newest
#1Claudia BusoneroH-Index: 8
#2Stefano LeoneH-Index: 20
Last. Filippo AcconciaH-Index: 30
view all 9 authors...
Estrogen receptor α expressing breast cancers (BC) are classically treated with endocrine therapy. Prolonged endocrine therapy often results in a metastatic disease (MBC), for which a standardized effective therapy is still lacking. Thus, new drugs are required for primary and metastatic BC treatment. Here, we report that the Food and Drug Administration (FDA)-approved drugs, ouabain and digoxin, induce ERα degradation and prevent proliferation in cells modeling primary and metastatic BC. Ouabai...
1 CitationsSource
The renin-angiotensin system (RAS) is a network of proteins regulating many aspects of human physiology, including cardiovascular, pulmonary, and immune system physiology. The RAS is a complicated network of G-protein coupled receptors (GPCRs) (i.e., AT1R, AT2R, MASR, and MRGD) orchestrating the effects of several hormones (i.e., angiotensin II, angiotensin (1–7), and alamandine) produced by protease-based transmembrane receptors (ACE1 and ACE2). Two signaling axes have been identified in the RA...
1 CitationsSource
17β-Estradiol (E2) controls diverse physiological processes, including cell proliferation, through its binding to estrogen receptor α (ERα). E2:ERα signaling depends on both the receptor subcellular localization (e.g., nucleus, plasma membrane) and intracellular ERα abundance. Indeed, the control of ERα levels is necessary for the effects of E2, and E2 itself induces ERα degradation and cell proliferation in parallel. Thus, the modulation of intracellular ERα levels is a critical parameter for E...
1 CitationsSource
Kinetic analyses of diverse physiological processes have the potential to unveil new aspects of the molecular regulation of cell biology at temporal levels. 17beta-estradiol (E2) regulates diverse physiological effects by binding to the estrogen receptor alpha (ERalpha), which primarily works as a transcription factor. Although many molecular details of the modulation of ERalpha transcriptional activity have been discovered including the impact of receptor plasma membrane localization and its re...
3 CitationsSource
#1Manuela CipollettiH-Index: 7
#2Stefano LeoneH-Index: 20
Last. Filippo AcconciaH-Index: 30
view all 5 authors...
Kinetic analyses of diverse physiological processes have the potential to unveil new aspects of the molecular regulation of cell biology at temporal levels. 17beta-estradiol (E2) regulates diverse physiological effects by binding to the estrogen receptor alpha (ERalpha), which primarily works as a transcription factor. Although many molecular details of the modulation of ERalpha transcriptional activity have been discovered including the impact of receptor plasma membrane localization and its re...
Source
Abstract With the advent of omic technologies, our understanding of the molecular mechanisms underlying estrogen receptor α (ERα)-expressing breast cancer (BC) progression has grown exponentially. Nevertheless, the most widely used therapy for inhibiting this disease is endocrine therapy (ET) (i.e., aromatase inhibitors, tamoxifen - Tam, faslodex/fulvestrant - FUL). However, in a considerable number of cases, prolonged patient treatment with ET generates the development of resistant tumor cells ...
13 CitationsSource
#1Claudia BusoneroH-Index: 8
#2Stefano LeoneH-Index: 20
Last. Filippo AcconciaH-Index: 30
view all 4 authors...
Purpose Most breast cancers (BCs) express estrogen receptor α (ERα) and are treated with the endocrine therapy (ET) drugs 4OH-tamoxifen (Tam) and fulvestrant (ICI 182,780; ICI). Unfortunately, a high fraction of ET treated women relapses and becomes resistant to ET. Therefore, additional anti-BC drugs are needed. Recently, we proposed that the identification of novel anti-BC drugs can be achieved using modulation of the intracellular ERα content in BC cells as a pharmacological target. Here, we ...
6 CitationsSource
#1Claudia BusoneroH-Index: 8
#2Stefano LeoneH-Index: 20
Last. Filippo AcconciaH-Index: 30
view all 4 authors...
Purpose: Most breast cancers (BCs) express estrogen receptor α (ERα) and are treated with the endocrine therapy (ET) drugs 4OH-tamoxifen (Tam) and fulvestrant (i.e., ICI182,780-ICI). Unfortunately, a high fraction of ET-treated women relapses and become resistant to ET. Therefore, additional anti-BC drugs are needed. Recently, we proposed that the identification of novel anti-BC drugs can be achieved using the modulation of the ERα intracellular content in BC cells as a pharmacological target. H...
1 CitationsSource
#1Stefano LeoneH-Index: 20
#2Claudia BusoneroH-Index: 8
Last. Filippo AcconciaH-Index: 30
view all 3 authors...
17β-estradiol (E2) regulates diverse physiological effects including cell proliferation through the estrogen receptor α (ERα), which as a transcription factor drives gene transcription and as an extra-nuclear localized receptor triggers the membrane-dependent activation of diverse kinase cascades. E2 also modifies ERα intracellular levels via diverse intracellular mechanisms. In this way, the E2-acivated ERα integrates signaling cascades with the modulation of receptor intracellular concentratio...
8 CitationsSource
Abstract Most cases of breast cancer (BC) are estrogen receptor α-positive (ERα+) at diagnosis. The presence of ERα drives the therapeutic approach for this disease, which often consists of endocrine therapy (ET). 4OH-Tamoxifen and faslodex (i.e., fulvestrant - ICI182,780) are two ETs that render tumor cells insensitive to 17β-estradiol (E2)-dependent proliferative stimuli and prevent BC progression. However, ET has limitations and serious failures in different tissues and organs. Thus, there is...
8 CitationsSource
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