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  1. Article: Interleukin-6 Function and Targeting in Prostate Cancer.

    Culig, Zoran

    Advances in experimental medicine and biology

    2021  Volume 1290, Page(s) 1–8

    Abstract: Interleukin-6 (IL-6) is a proinflammatory cytokine, which is involved in pathogenesis of several cancers. Its expression and function in prostate cancer have been extensively studied in cellular models and clinical specimens. High levels of IL-6 were ... ...

    Abstract Interleukin-6 (IL-6) is a proinflammatory cytokine, which is involved in pathogenesis of several cancers. Its expression and function in prostate cancer have been extensively studied in cellular models and clinical specimens. High levels of IL-6 were detected in conditioned media from cells which do not respond to androgens. Increased phosphorylation of signal transducer and activator of transcription (STAT)3 factor which is induced in response to IL-6 is one of the typical features of prostate cancer. However, reports in the literature show regulation of neuroendocrine phenotype by IL-6. Effects of IL-6 on stimulation of proliferation, migration, and invasion lead to the establishment of experimental and clinical approaches to target IL-6. In prostate cancer, anti-IL-6 antibodies were demonstrated to inhibit growth in vitro and in vivo. Clinically, application of anti-IL-6 therapies did not improve survival of patients with metastatic prostate cancer. However, clinical trial design in the future may include different treatment schedule and combinations with experimental and clinical therapies. Endogenous inhibitors of IL-6 such as suppressors of cytokine signaling and protein inhibitors of activated STAT have variable effects on prostate cells, depending on presence or absence of the androgen receptor.
    MeSH term(s) Humans ; Interleukin-6/metabolism ; Male ; Phosphorylation ; Prostatic Neoplasms/drug therapy ; STAT3 Transcription Factor/genetics
    Chemical Substances Interleukin-6 ; STAT3 Transcription Factor
    Language English
    Publishing date 2021-02-09
    Publishing country United States
    Document type Journal Article
    ISSN 2214-8019 ; 0065-2598
    ISSN (online) 2214-8019
    ISSN 0065-2598
    DOI 10.1007/978-3-030-55617-4_1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Response to Androgens and Androgen Receptor Antagonists in the Presence of Cytokines in Prostate Cancer.

    Culig, Zoran

    Cancers

    2021  Volume 13, Issue 12

    Abstract: Non-steroidal anti-androgens have a major role in the treatment of non-localized prostate cancer. Interleukins are involved in the regulation of many cellular functions in prostate cancer and also modify cellular response to anti-androgens. A specific ... ...

    Abstract Non-steroidal anti-androgens have a major role in the treatment of non-localized prostate cancer. Interleukins are involved in the regulation of many cellular functions in prostate cancer and also modify cellular response to anti-androgens. A specific role of selected IL is presented in this review. IL-8 is a cytokine expressed in prostate cancer tissue and microenvironment and promotes proliferation and androgen receptor-mediated transcription. In contrast, IL-1 displays negative effects on expression of androgen receptor and its target genes. A subgroup of prostate cancers show neuroendocrine differentiation, which may be in part stimulated by androgen ablation. A similar effect was observed after treatment of cells with IL-10. Another cytokine which is implicated in regulation of androgenic response is IL-23, secreted by myeloid cells. Most studies on androgens and IL were carried out with IL-6, which acts through the signal transducer and activator of the transcription (STAT) factor pathway. IL-6 is implicated in resistance to enzalutamide. Activation of the STAT-3 pathway is associated with increased cellular stemness. IL-6 activation of the androgen receptor in some prostate cancers is associated with increased growth in vitro and in vivo. Molecules such as galiellalactone or niclosamide have an inhibitory effect on both androgen receptor and STAT-3 pathways.
    Language English
    Publishing date 2021-06-12
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers13122944
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  3. Article ; Online: miRNA as Regulators of Prostate Carcinogenesis and Endocrine and Chemoresistance.

    Culig, Zoran

    Current cancer drug targets

    2021  Volume 21, Issue 4, Page(s) 283–288

    Abstract: More therapy options are available for advanced prostate cancer, including novel inhibitors of androgen synthesis, anti-androgens, chemotherapeutics and targeted therapies. Although patients ´ survival has been improved, management of castration therapy- ... ...

    Abstract More therapy options are available for advanced prostate cancer, including novel inhibitors of androgen synthesis, anti-androgens, chemotherapeutics and targeted therapies. Although patients ´ survival has been improved, management of castration therapy-resistant prostate cancer remains a challenge. Regulation of cellular events in cancer by small non-coding miRNAs is, therefore, an area of special interest. Overexpression of selected miRNA may lead to androgen independence and prostate cancer progression. miRNA may be considered also a biomarker in patients with prostate cancer. In contrast, diminished expression of tumor-suppressive miRNA in prostate cancer leads to enhanced proliferation, reduced apoptosis, increased migration, invasion and epithelial- to-mesenchymal transition. miRNA may be directly involved in the regulation of chemosensitivity in prostate cancer. Experimental overexpression of selected miRNA in chemoresistant prostate cancer leads to the inhibition of cellular stemness and epithelial-to-mesenchymal transition. Reduction of tumor-suppressive miRNA may also lead to hyperactivity of signaling pathways such as that of the epidermal growth factor receptor and mitogen-activated protein kinase. Although considerable progress on miRNA research in prostate cancer has been achieved, therapeutic effects could be improved on the basis of the development of novel delivery methods.
    MeSH term(s) Androgen Antagonists/pharmacology ; Antineoplastic Agents/pharmacology ; Biomarkers, Tumor/genetics ; Carcinogenesis/genetics ; Disease Progression ; Drug Resistance, Neoplasm/genetics ; Humans ; Male ; MicroRNAs/genetics ; Molecular Targeted Therapy/methods ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Prostatic Neoplasms, Castration-Resistant/genetics
    Chemical Substances Androgen Antagonists ; Antineoplastic Agents ; Biomarkers, Tumor ; MicroRNAs
    Language English
    Publishing date 2021-01-10
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 2064824-8
    ISSN 1873-5576 ; 1568-0096
    ISSN (online) 1873-5576
    ISSN 1568-0096
    DOI 10.2174/1568009620666210108103134
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    Zs.A 5589: Show issues Location:
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  4. Article ; Online: Clinical and basic research implications of the article 'IGF-1 axis changes with ADT and docetaxel in metastatic prostate cancer'.

    Heidegger, Isabel / Culig, Zoran

    Endocrine-related cancer

    2024  Volume 31, Issue 5

    MeSH term(s) Male ; Humans ; Docetaxel/therapeutic use ; Insulin-Like Growth Factor I ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/pathology ; Androgen Antagonists/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols ; Treatment Outcome
    Chemical Substances Docetaxel (15H5577CQD) ; Insulin-Like Growth Factor I (67763-96-6) ; Androgen Antagonists
    Language English
    Publishing date 2024-03-22
    Publishing country England
    Document type Journal Article
    ZDB-ID 1218450-0
    ISSN 1479-6821 ; 1351-0088
    ISSN (online) 1479-6821
    ISSN 1351-0088
    DOI 10.1530/ERC-23-0362
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  5. Article ; Online: Androgen Receptor-Interacting Proteins in Prostate Cancer Development and Therapy Resistance.

    Culig, Zoran / Puhr, Martin

    The American journal of pathology

    2023  Volume 194, Issue 3, Page(s) 324–334

    Abstract: Endocrine therapy for prostate cancer is based on the use of drugs that diminish androgen concentration and androgen receptor (AR) signaling inhibitors and is limited by the functional consequences of AR point mutations and increased expression of ... ...

    Abstract Endocrine therapy for prostate cancer is based on the use of drugs that diminish androgen concentration and androgen receptor (AR) signaling inhibitors and is limited by the functional consequences of AR point mutations and increased expression of constitutively active receptors. Many coactivators (>280) interact with different AR regions. Most studies have determined the expression of coactivators and their effects in the presence of increasing concentrations of androgen or the antiandrogen enzalutamide. The p160 group of coactivators (SRC-1, SRC-2, and SRC-3) is highly expressed in prostate cancer and contributes to ligand-dependent activation of the receptor in models that represent therapy-sensitive and therapy-resistant cell lines. The transcriptional coactivators p300 and CREB-binding protein (CBP) are implicated in the regulation of a large number of cellular events, such as proliferation, apoptosis, migration, and invasion. AR coactivators also may predict biochemical and clinical recurrence. The AR coactivator expression, which is enhanced in enzalutamide resistance, includes growth regulating estrogen receptor binding 1 (GREB1) and GATA-binding protein 2 (GATA2). Several coactivators also activate AR-unrelated signaling pathways, such as those of insulin-like growth factors, which inhibit apoptosis in cancer cells. They are expressed in multiple models of resistance to therapy and can be targeted by various inhibitors in vitro and in vivo. The role of the glucocorticoid receptor in endocrine therapy-resistant prostate cancer has been documented previously. Specific coactivators may interact with the glucocorticoid receptor, thus contributing to therapy failure.
    MeSH term(s) Male ; Humans ; Androgens/metabolism ; Receptors, Androgen/genetics ; Receptors, Androgen/metabolism ; Receptors, Glucocorticoid ; Histone Acetyltransferases ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/genetics ; Cell Line, Tumor ; Benzamides ; Nitriles ; Phenylthiohydantoin
    Chemical Substances Androgens ; enzalutamide (93T0T9GKNU) ; Receptors, Androgen ; Receptors, Glucocorticoid ; Histone Acetyltransferases (EC 2.3.1.48) ; Benzamides ; Nitriles ; Phenylthiohydantoin (2010-15-3)
    Language English
    Publishing date 2023-12-15
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2943-9
    ISSN 1525-2191 ; 0002-9440
    ISSN (online) 1525-2191
    ISSN 0002-9440
    DOI 10.1016/j.ajpath.2023.12.003
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  6. Article ; Online: IL-6 causes multiple effects in androgen-sensitive and -insensitive prostate cancer cell lines.

    Culig, Zoran

    Expert review of endocrinology & metabolism

    2019  Volume 6, Issue 3, Page(s) 327–332

    Abstract: The androgen receptor (AR) is expressed in most human prostate cancers. It can be activated in a hypersensitive manner by androgens, nonandrogenic steroids, nonsteroidal anti-androgens and in a ligand-independent manner. IL-6 is a proinflammatory ... ...

    Abstract The androgen receptor (AR) is expressed in most human prostate cancers. It can be activated in a hypersensitive manner by androgens, nonandrogenic steroids, nonsteroidal anti-androgens and in a ligand-independent manner. IL-6 is a proinflammatory cytokine that activates several signaling pathways. It can either stimulate or inhibit growth of prostate cancer cells. IL-6 is an important positive regulator of AR activity and can stimulate the expression of prostate-specific antigen in a ligand-independent manner. IL-6/AR interaction may either result in growth stimulation (MDA PCa 2b cells) or inhibition (LAPC-4 cells). IL-8 and IL-4 have also been observed to activate AR. Cells generated by prolonged treatment with IL-6 acquire a growth advantage. There are several therapeutic options to target IL-6 in prostate cancer and most laboratory studies have been performed with the monoclonal antibody siltuximab. Endogenous suppressors of cytokine signaling (SOCS)-3 and -1 are expressed in prostate cancer tissue. SOCS-3 inhibits apoptosis in AR-negative cells. However, in androgen-sensitive prostate cancer cell lines, SOCS-3 is induced by androgen and blocks its effects on proliferation and secretion. It is currently understood that there are numerous interactions between androgen and IL-6 signaling in human prostate cancer.
    Language English
    Publishing date 2019-02-12
    Publishing country England
    Document type Journal Article
    ISSN 1744-8417
    ISSN (online) 1744-8417
    DOI 10.1586/eem.11.34
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  7. Article ; Online: Centrosomal Proteins in Urothelial Tumors: New Pathways in Disease Pathogenesis.

    Culig, Zoran

    The American journal of pathology

    2019  Volume 189, Issue 6, Page(s) 1178–1179

    Abstract: This commentary highlights the article by Li et al that identified the centrosomal protein 72 as a biomarker for prognosis of urothelial cancer. ...

    Abstract This commentary highlights the article by Li et al that identified the centrosomal protein 72 as a biomarker for prognosis of urothelial cancer.
    MeSH term(s) Carcinoma, Transitional Cell ; Epigenesis, Genetic ; Humans ; Microtubule-Associated Proteins ; Plasminogen Activator Inhibitor 1 ; Prognosis ; Urinary Bladder Neoplasms
    Chemical Substances CEP72 protein, human ; Microtubule-Associated Proteins ; Plasminogen Activator Inhibitor 1 ; SERPINE1 protein, human
    Language English
    Publishing date 2019-04-13
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2943-9
    ISSN 1525-2191 ; 0002-9440
    ISSN (online) 1525-2191
    ISSN 0002-9440
    DOI 10.1016/j.ajpath.2019.04.002
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  8. Article ; Online: Epithelial mesenchymal transition and resistance in endocrine-related cancers.

    Culig, Zoran

    Biochimica et biophysica acta. Molecular cell research

    2019  Volume 1866, Issue 9, Page(s) 1368–1375

    Abstract: Epithelial to mesencyhmal transition (EMT) has a central role in tumor metastasis and progression. EMT is regulated by several growth factors and pro-inflammatory cytokines. The most important role in this regulation could be attributed to transforming ... ...

    Abstract Epithelial to mesencyhmal transition (EMT) has a central role in tumor metastasis and progression. EMT is regulated by several growth factors and pro-inflammatory cytokines. The most important role in this regulation could be attributed to transforming growth factor-β (TGF-β). In breast cancer, TGF-β effect on EMT could be potentiated by Fos-related antigen, oncogene HER2, epidermal growth factor, or mitogen-activated protein kinase kinase 5 - extracellular-regulated kinase signaling. Several microRNAs in breast cancer have a considerable role either in potentiation or in suppression of EMT thus acting as oncogenic or tumor suppressive modulators. At present, possibilities to target EMT are discussed but the results of clinical translation are still limited. In prostate cancer, many cellular events are regulated by androgenic hormones. Different experimental results on androgenic stimulation or inhibition of EMT have been reported in the literature. Thus, a possibility that androgen ablation therapy leads to EMT thus facilitating tumor progression has to be discussed. Novel therapy agents, such as the anti-diabetic drug metformin or selective estrogen receptor modulator ormeloxifene were used in pre-clinical studies to inhibit EMT in prostate cancer. Taken together, the results of pre-clinical and clinical studies in breast cancer may be helpful in the process of drug development and identify potential risk during the early stage of that process.
    MeSH term(s) Benzopyrans/pharmacology ; Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Cadherins/metabolism ; Cadherins/pharmacology ; Cell Plasticity/drug effects ; Cytokines ; Disease Progression ; Epidermal Growth Factor ; Epithelial-Mesenchymal Transition/drug effects ; Epithelial-Mesenchymal Transition/physiology ; Female ; Humans ; Inflammation ; MAP Kinase Kinase 5 ; Male ; Metformin/pharmacology ; MicroRNAs/metabolism ; MicroRNAs/pharmacology ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/metabolism ; Proto-Oncogene Proteins c-fos ; Receptor, ErbB-2 ; Signal Transduction ; Transforming Growth Factor beta/metabolism ; Transforming Growth Factor beta/pharmacology
    Chemical Substances Benzopyrans ; Cadherins ; Cytokines ; MicroRNAs ; Proto-Oncogene Proteins c-fos ; Transforming Growth Factor beta ; ormeloxifene (44AXY5VE90) ; Epidermal Growth Factor (62229-50-9) ; Metformin (9100L32L2N) ; ERBB2 protein, human (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1) ; MAP Kinase Kinase 5 (EC 2.7.12.2) ; MAP2K5 protein, human (EC 2.7.12.2)
    Language English
    Publishing date 2019-05-18
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 60-7
    ISSN 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbamcr.2019.05.003
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  9. Article: Das Beste aus der Grundlagenforschung zum Prostatakarzinom

    Culig, Z.

    Urologik

    2019  Volume 26, Issue 2, Page(s) 12

    Language German
    Document type Article
    ZDB-ID 2065143-0
    ISSN 1561-526X
    Database Current Contents Medicine

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    Zs.A 5597: Show issues Location:
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  10. Article ; Online: The way towards understanding possible multiple functions of AR V7 in prostate cancer.

    Culig, Zoran

    BJU international

    2018  Volume 122, Issue 2, Page(s) 169

    MeSH term(s) Humans ; Male ; Prostatic Neoplasms, Castration-Resistant ; Receptors, Androgen
    Chemical Substances Receptors, Androgen
    Language English
    Publishing date 2018-08-21
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 1462191-5
    ISSN 1464-410X ; 1464-4096 ; 1358-8672
    ISSN (online) 1464-410X
    ISSN 1464-4096 ; 1358-8672
    DOI 10.1111/bju.14406
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