Prolactin receptor targeting in breast and prostate cancers: New insights into an old challenge

Goffin, Vincent

doi:10.1016/j.pharmthera.2017.05.009

Cited by 62 publications

(54 citation statements)

References 190 publications

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“…On the other hand, top to 70% of patients with breast cancer brain metastases (BCBM) show the activated PI3K pathway [170], and GDC-0084 induces apoptosis of PIK3CA-mutant BCBM cells by suppressing activation of AKT and p70 S6 kinase [171]. Additionally, PRLR/Jak2/STAT5 is the main signaling pathway for activation in mammary gland, and PRLR-triggered pro-tumorigenic pathways in BC include the PI3K/AKT pathway [172]. As well, numerous studies have shown that IRS4, CDK12, SPC24, Mfng, Transgelin 2, STX3, SOX4, PAK4, TPX2, MEG3 and miR-21, -93, -106b, -130b, -214, -361-5p, -489, -511, -564 as well as lncRNA-HOTAIR and MALAT1 regulate tumorigenesis, proliferation, apoptosis, invasion, migration, paclitaxel resistance or anti-Her2 therapy (trastuzumab) resistance of BC cells through PI3K/AKT pathway [173][174][175][176][177][178][179][180][181][182][183][184][185][186][187][188][189][190][191].…”

Section: Nct02240212mentioning

confidence: 99%

“…Sexual hormones have been historically associated with PCa for the androgen deprivation therapy (ADT), but scientific evidences including the increasingly emerging of castration resistant prostate cancer (CRPC) are inconsistent to decide whether their involvement is aetiological or a phenotype component of the disease. However, similar to BC, PRLR/ Jak2/STAT5 is also the main signaling pathway for activation in prostate gland, and PRLR-triggered pro-tumorigenic pathways in PCa include PI3K/AKT [172]. In addition, AEP, SCL/TAL1, SIRT3, Snail, MED15, STIM1, ST6Gal-I, Glyoxalase 2, ASF1B, GPCR48/LGR4, AP4, GCN5, SAG/ RBX2 E3, miR-7, -101, -129, -133a-3p, and -4638-5p, as well as LncRNA HCG11 and ATB govern tumorigenesis, progression, metastasis, EMT or castration resistant of PCa cells via PI3K/AKT pathway [237][238][239][240][241][242][243][244][245][246][247][248][249][250][251][252][253][254][255][256].…”

Section: Dysregulation Of the Pi3k/akt Pathway In The Genitourinary Smentioning

confidence: 99%

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Role of PI3K/AKT pathway in cancer: the framework of malignant behavior

et al. 2020

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Given that the PI3K/AKT pathway has manifested its compelling influence on multiple cellular process, we further review the roles of hyperactivation of PI3K/AKT pathway in various human cancers. We state the abnormalities of PI3K/AKT pathway in different cancers, which are closely related with tumorigenesis, proliferation, growth, apoptosis, invasion, metastasis, epithelial-mesenchymal transition, stem-like phenotype, immune microenvironment and drug resistance of cancer cells. In addition, we investigated the current clinical trials of inhibitors against PI3K/AKT pathway in cancers and found that the clinical efficacy of these inhibitors as monotherapy has so far been limited despite of the promising preclinical activity, which means combinations of targeted therapy may achieve better efficacies in cancers. In short, we hope to feature PI3K/ AKT pathway in cancers to the clinic and bring the new promising to patients for targeted therapies.

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Section: Nct02240212mentioning

confidence: 99%

Section: Dysregulation Of the Pi3k/akt Pathway In The Genitourinary Smentioning

confidence: 99%

Role of PI3K/AKT pathway in cancer: the framework of malignant behavior

et al. 2020

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“…An association with PRL levels and breast [156][157][158], ovarian [159], colon [160,161] and hepatocellular [162] cancer has been suggested. Although basic science studies have implicated a role for PRL and its receptor in the pathogenesis of different malignancies [157,158,[163][164][165][166], a clear causal relationship between PRL and cancer remains controversial [158]. Epidemiological studies on this topic have shown conflicting results [158], and reports suggesting positive association between PRL values and cancer risk should be interpreted with caution, as some include individuals with normal PRL values, or rely on a single measurement of the hormone [156][157][158].…”

Section: Cancermentioning

confidence: 99%

Hyperprolactinaemia

Samperi

Lithgow

Karavitaki

2019

JCM

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Hyperprolactinaemia is one of the most common problems in clinical endocrinology. It relates with various aetiologies (physiological, pharmacological, pathological), the clarification of which requires careful history taking and clinical assessment. Analytical issues (presence of macroprolactin or of the hook effect) need to be taken into account when interpreting the prolactin values. Medications and sellar/parasellar masses (prolactin secreting or acting through "stalk effect") are the most common causes of pathological hyperprolactinaemia. Hypogonadism and galactorrhoea are well-recognized manifestations of prolactin excess, although its implications on bone health, metabolism and immune system are also expanding. Treatment mainly aims at restoration and maintenance of normal gonadal function/fertility, and prevention of osteoporosis; further specific management strategies depend on the underlying cause. In this review, we provide an update on the diagnostic and management approaches for the patient with hyperprolactinaemia and on the current data looking at the impact of high prolactin on metabolism, cardiovascular and immune systems.

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“…This has resulted in erroneous and untenable views that prolactin regulation of all prostate functions occur via the complex cytokine pathway. This is apparent from conclusions in contemporary reports and reviews (such as 15 ) that STAT5 is the only PRLR signaling pathway that is activated to detectable levels by PRL in the prostate .…”

Section: Testosterone and Prolactin; The Major Endocrine Regulation Omentioning

confidence: 99%

Testosterone, prolactin, and oncogenic regulation of the prostate gland. A new concept: Testosterone-independent malignancy is the development of prolactin-dependent malignancy!

Costello

Franklin

2018

Oncol Rev

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Hormone-independent malignancy is a major issue of morbidity and deaths that confronts prostate cancer. Despite decades of research, the oncogenic and hormonal implications in the development and progression of prostate malignancy remain mostly speculative. This is largely due to the absence and/or lack of consideration by contemporary clinicians and biomedical investigators regarding the established implications of the co-regulation of testosterone and prolactin in the development, maintenance, metabolism and functions of the prostate gland. Especially relevant is the major metabolic function of production of high levels of citrate by the peripheral zone acinar epithelial cells. Citrate production, along with growth and proliferation by these cells, is regulated by co-existing testosterone and prolactin signaling pathways; and by the oncogenic down-regulation of ZIP1 transporter/zinc/citrate in the development of malignancy. These relationships had not been considered in the issues of hormonedependent malignancy.This review provides the relevant background that has established the dual role of testosterone and prolactin regulation of the prostate gland; which is essential to address the implications in the oncogenic development and progression of hormone-dependent malignancy. The oncogenic factor along with testosterone-dependent and prolactin-dependent relationships leads to the plausible concept that androgen ablation for the treatment of testosteronedependent malignancy results in the development of prolactindependent malignancy; which is testosterone-independent malignancy. Consequently, both testosterone ablation and prolactin ablation are required to prevent and/or abort terminal hormonedependent prostate cancer.

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Prolactin receptor targeting in breast and prostate cancers: New insights into an old challenge

Cited by 62 publications

References 190 publications

Role of PI3K/AKT pathway in cancer: the framework of malignant behavior

Role of PI3K/AKT pathway in cancer: the framework of malignant behavior

Hyperprolactinaemia

Testosterone, prolactin, and oncogenic regulation of the prostate gland. A new concept: Testosterone-independent malignancy is the development of prolactin-dependent malignancy!

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