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  1. Book: Phosphoinositide 3-kinase signalling pathway

    Lam, Eric W.-F.

    the key to cell proliferation and death

    2006  

    Author's details Eric W.-F. Lam
    Language English
    Size XIII, 238 S. : Ill., graph. Darst.
    Publisher Imperial College Press
    Publishing place London
    Publishing country Great Britain
    Document type Book
    HBZ-ID HT014733240
    ISBN 1-86094-626-7 ; 978-1-86094-626-4
    Database Catalogue ZB MED Medicine, Health

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  2. Article ; Online: Lysophosphatidic Acid Signalling Regulates Human Sperm Viability via the Phosphoinositide 3-Kinase/AKT Pathway.

    Liao, Hao-Yu / O'Flaherty, Cristian

    Cells

    2023  Volume 12, Issue 17

    Abstract: Lysophosphatidic acid (LPA) signalling is essential for maintaining germ cell viability during ...

    Abstract Lysophosphatidic acid (LPA) signalling is essential for maintaining germ cell viability during mouse spermatogenesis; however, its role in human spermatozoa is unknown. We previously demonstrated that peroxiredoxin 6 (PRDX6) calcium-independent phospholipase A
    MeSH term(s) Humans ; Male ; Lysophospholipids/pharmacology ; Peroxiredoxin VI ; Phosphatidylinositol 3-Kinases ; Proto-Oncogene Proteins c-akt ; Semen
    Chemical Substances lysophosphatidic acid (PG6M3969SG) ; Lysophospholipids ; Peroxiredoxin VI (EC 1.11.1.15) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2023-09-02
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12172196
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Trehalose hydrolysis and transport-related genes promote Bombyx mori nucleopolyhedrovirus proliferation through the phosphoinositide 3-kinase-Akt signalling pathway in BmN cell.

    Wang, Jie / Zhu, Han-Dan / Wang, Yan-Xiang / Guo, Zhe-Xiao / Liu, Ying-Xue / Huang, Zhi-Hao / Zhu, Lin-Bao / Liu, Ming-Hui / Liu, Shi-Huo / Xu, Jia-Ping

    Developmental and comparative immunology

    2022  Volume 140, Page(s) 104625

    Abstract: ... the expression of BmPI3K, BmPDK1 and BmAkt and inhibit the expression of BmFoxO in the phosphoinositide 3-kinase ... PI3K)-Akt signalling pathway. Similarly, the increased trehalose level in BmN cells could promote ... Akt signalling pathway to facilitate BmNPV proliferation. These findings help clarify the relationship ...

    Abstract The reprogramming of host physiology has been considered an essential process for baculovirus propagation. Trehalose, the main sugar in insect blood, plays a crucial role as an instant energy source. Although the trehalose level is modulated following infection with Bombyx mori nucleopolyhedrovirus (BmNPV), the mechanism of trehalose metabolism in response to BmNPV infection is still unclear. In this study, we demonstrated that the trehalose level tended to be lower in BmNPV-infected hemolymph and higher in the midgut. The omics analysis revealed that two trehalose transporters, BmTret1-1 and BmTret1-2, and trehalase, BmTRE1 and BmTRE2, were differentially expressed in the midgut after BmNPV infection. BmTret1-1 and BmTret1-2 had the ability to transport trehalose into the cell and promoted cellular absorption of trehalose. Furthermore, the functions of BmTret1-1, BmTret1-2, BmTRE1 and BmTRE2 in BmNPV infection were analyzed. These genes were upregulated in the midgut after BmNPV infection. Virus amplification analysis revealed that these genes could promote BmNPV proliferation in BmN cells. In addition, these genes could promote the expression of BmPI3K, BmPDK1 and BmAkt and inhibit the expression of BmFoxO in the phosphoinositide 3-kinase (PI3K)-Akt signalling pathway. Similarly, the increased trehalose level in BmN cells could promote the expression of BmPI3K, BmPDK1 and BmAkt and inhibit the expression of BmFoxO. Taken together, BmNPV infection promote the expression of trehalose hydrolysis and transport-related genes. These changes affect the PI3K-Akt signalling pathway to facilitate BmNPV proliferation. These findings help clarify the relationship between trehalose metabolism and BmNPV infection.
    MeSH term(s) Animals ; Phosphatidylinositol 3-Kinases/metabolism ; Hydrolysis ; Proto-Oncogene Proteins c-akt/metabolism ; Trehalose/metabolism ; Cell Proliferation ; Bombyx ; Insect Proteins/genetics ; Insect Proteins/metabolism
    Chemical Substances Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Trehalose (B8WCK70T7I) ; Insect Proteins
    Language English
    Publishing date 2022-12-23
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 752411-0
    ISSN 1879-0089 ; 0145-305X
    ISSN (online) 1879-0089
    ISSN 0145-305X
    DOI 10.1016/j.dci.2022.104625
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Inhibitors of phosphoinositide 3-kinase (PI3K) and phosphoinositide 3-kinase-related protein kinase family (PIKK).

    Huang, Xueqin / You, Li / Nepovimova, Eugenie / Psotka, Miroslav / Malinak, David / Valko, Marian / Sivak, Ladislav / Korabecny, Jan / Heger, Zbynek / Adam, Vojtech / Wu, Qinghua / Kuca, Kamil

    Journal of enzyme inhibition and medicinal chemistry

    2023  Volume 38, Issue 1, Page(s) 2237209

    Abstract: Phosphoinositide 3-kinases (PI3K) and phosphoinositide 3-kinase-related protein kinases (PIKK) are ... repair. Dysfunction of PIKK members and aberrant stimulation of the PI3K/AKT/mTOR signalling pathway are ... two structurally related families of kinases that play vital roles in cell growth and DNA damage ...

    Abstract Phosphoinositide 3-kinases (PI3K) and phosphoinositide 3-kinase-related protein kinases (PIKK) are two structurally related families of kinases that play vital roles in cell growth and DNA damage repair. Dysfunction of PIKK members and aberrant stimulation of the PI3K/AKT/mTOR signalling pathway are linked to a plethora of diseases including cancer. In recent decades, numerous inhibitors related to the PI3K/AKT/mTOR signalling have made great strides in cancer treatment, like copanlisib and sirolimus. Notably, most of the PIKK inhibitors (such as VX-970 and M3814) related to DNA damage response have also shown good efficacy in clinical trials. However, these drugs still require a suitable combination therapy to overcome drug resistance or improve antitumor activity. Based on the aforementioned facts, we summarised the efficacy of PIKK, PI3K, and AKT inhibitors in the therapy of human malignancies and the resistance mechanisms of targeted therapy, in order to provide deeper insights into cancer treatment.
    MeSH term(s) Humans ; Phosphatidylinositol 3-Kinase/metabolism ; Phosphatidylinositol 3-Kinase/therapeutic use ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Phosphoinositide-3 Kinase Inhibitors/pharmacology ; TOR Serine-Threonine Kinases/metabolism ; Neoplasms/drug therapy ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use
    Chemical Substances Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Phosphoinositide-3 Kinase Inhibitors ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Protein Kinase Inhibitors
    Language English
    Publishing date 2023-07-24
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2082578-X
    ISSN 1475-6374 ; 1475-6366
    ISSN (online) 1475-6374
    ISSN 1475-6366
    DOI 10.1080/14756366.2023.2237209
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Trehalose hydrolysis and transport–related genes promote Bombyx mori nucleopolyhedrovirus proliferation through the phosphoinositide 3-kinase–Akt signalling pathway in BmN cell

    Wang, Jie / Zhu, Han-Dan / Wang, Yan-Xiang / Guo, Zhe-Xiao / Liu, Ying-Xue / Huang, Zhi-Hao / Zhu, Lin-Bao / Liu, Minghui / Liu, Shi-Huo / Xu, Jia-Ping

    Developmental and Comparative Immunology. 2023 Mar., v. 140 p.104625-

    2023  

    Abstract: ... the expression of BmPI3K, BmPDK1 and BmAkt and inhibit the expression of BmFoxO in the phosphoinositide 3-kinase ... PI3K)–Akt signalling pathway. Similarly, the increased trehalose level in BmN cells could promote ... Akt signalling pathway to facilitate BmNPV proliferation. These findings help clarify the relationship ...

    Abstract The reprogramming of host physiology has been considered an essential process for baculovirus propagation. Trehalose, the main sugar in insect blood, plays a crucial role as an instant energy source. Although the trehalose level is modulated following infection with Bombyx mori nucleopolyhedrovirus (BmNPV), the mechanism of trehalose metabolism in response to BmNPV infection is still unclear. In this study, we demonstrated that the trehalose level tended to be lower in BmNPV-infected hemolymph and higher in the midgut. The omics analysis revealed that two trehalose transporters, BmTret1-1 and BmTret1-2, and trehalase, BmTRE1 and BmTRE2, were differentially expressed in the midgut after BmNPV infection. BmTret1-1 and BmTret1-2 had the ability to transport trehalose into the cell and promoted cellular absorption of trehalose. Furthermore, the functions of BmTret1-1, BmTret1-2, BmTRE1 and BmTRE2 in BmNPV infection were analyzed. These genes were upregulated in the midgut after BmNPV infection. Virus amplification analysis revealed that these genes could promote BmNPV proliferation in BmN cells. In addition, these genes could promote the expression of BmPI3K, BmPDK1 and BmAkt and inhibit the expression of BmFoxO in the phosphoinositide 3-kinase (PI3K)–Akt signalling pathway. Similarly, the increased trehalose level in BmN cells could promote the expression of BmPI3K, BmPDK1 and BmAkt and inhibit the expression of BmFoxO. Taken together, BmNPV infection promote the expression of trehalose hydrolysis and transport–related genes. These changes affect the PI3K–Akt signalling pathway to facilitate BmNPV proliferation. These findings help clarify the relationship between trehalose metabolism and BmNPV infection.
    Keywords Bombyx mori nucleopolyhedrovirus ; absorption ; blood ; energy ; hemolymph ; hydrolysis ; immunology ; insects ; metabolism ; midgut ; phosphatidylinositol 3-kinase ; trehalase ; trehalose ; viruses ; Bombyx mori ; Trehalose hydrolysis and transport ; B. mori nucleopolyhedrovirus ; PI3K-Akt signalling pathway
    Language English
    Dates of publication 2023-03
    Publishing place Elsevier Ltd
    Document type Article ; Online
    ZDB-ID 752411-0
    ISSN 1879-0089 ; 0145-305X
    ISSN (online) 1879-0089
    ISSN 0145-305X
    DOI 10.1016/j.dci.2022.104625
    Database NAL-Catalogue (AGRICOLA)

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  6. Article ; Online: Phosphoinositide 3-kinase signalling in the nucleolus.

    Morovicz, Andrea Papdiné / Mazloumi Gavgani, Fatemeh / Jacobsen, Rhîan G / Skuseth Slinning, Malene / Turcu, Diana C / Lewis, Aurélia E

    Advances in biological regulation

    2021  Volume 83, Page(s) 100843

    Abstract: The phosphoinositide 3-kinase (PI3K) signalling pathway plays key roles in many cellular processes ... of downstream phosphatidylinositol (3,4,5)trisphosphate effector proteins. ... focuses on nucleolar PI3K signalling and how it regulates rRNA synthesis, as well as on the identification ...

    Abstract The phosphoinositide 3-kinase (PI3K) signalling pathway plays key roles in many cellular processes and is altered in many diseases. The function and mode of action of the pathway have mostly been elucidated in the cytoplasm. However, many of the components of the PI3K pathway are also present in the nucleus at specific sub-nuclear sites including nuclear speckles, nuclear lipid islets and the nucleolus. Nucleoli are membrane-less subnuclear structures where ribosome biogenesis occurs. Processes leading to ribosome biogenesis are tightly regulated to maintain protein translation capacity of cells. This review focuses on nucleolar PI3K signalling and how it regulates rRNA synthesis, as well as on the identification of downstream phosphatidylinositol (3,4,5)trisphosphate effector proteins.
    MeSH term(s) Cell Nucleolus/genetics ; Cell Nucleolus/metabolism ; Cell Nucleus/genetics ; Cell Nucleus/metabolism ; Humans ; Phosphatidylinositol 3-Kinase/metabolism ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Signal Transduction
    Chemical Substances Phosphatidylinositol 3-Kinase (EC 2.7.1.137)
    Language English
    Publishing date 2021-12-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2667413-0
    ISSN 2212-4934 ; 2212-4926
    ISSN (online) 2212-4934
    ISSN 2212-4926
    DOI 10.1016/j.jbior.2021.100843
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Phosphoinositide 3-Kinase-Dependent Signalling Pathways in Cutaneous Squamous Cell Carcinomas.

    Janus, Joanna M / O'Shaughnessy, Ryan F L / Harwood, Catherine A / Maffucci, Tania

    Cancers

    2017  Volume 9, Issue 7

    Abstract: ... some of the evidence indicating that activation of phosphoinositide 3-kinases (PI3Ks)-dependent signalling pathways ... suggesting that inhibition of these pathways can be beneficial to counteract the disease. With the growing ... the specific contribution of distinct components of the PI3Ks/Akt/mTOR pathways in order to identify the most ...

    Abstract Cutaneous squamous cell carcinoma (cSCC) derives from keratinocytes in the epidermis and accounts for 15-20% of all cutaneous malignancies. Although it is usually curable by surgery, 5% of these tumours metastasise leading to poor prognosis mostly because of a lack of therapies and validated biomarkers. As the incidence rate is rising worldwide it has become increasingly important to better understand the mechanisms involved in cSCC development and progression in order to develop therapeutic strategies. Here we discuss some of the evidence indicating that activation of phosphoinositide 3-kinases (PI3Ks)-dependent signalling pathways (in particular the PI3Ks targets Akt and mTOR) has a key role in cSCC. We further discuss available data suggesting that inhibition of these pathways can be beneficial to counteract the disease. With the growing number of different inhibitors currently available, it would be important to further investigate the specific contribution of distinct components of the PI3Ks/Akt/mTOR pathways in order to identify the most promising molecular targets and the best strategy to inhibit cSCC.
    Language English
    Publishing date 2017-07-11
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers9070086
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Class I Phosphoinositide 3-Kinase

    Mazloumi Gavgani, Fatemeh / Smith Arnesen, Victoria / Jacobsen, Rhîan G / Krakstad, Camilla / Hoivik, Erling A / Lewis, Aurélia E

    International journal of molecular sciences

    2018  Volume 19, Issue 12

    Abstract: The phosphoinositide 3-kinase (PI3K) signalling pathway is highly dysregulated in cancer, leading ... to elevated PI3K signalling and altered cellular processes that contribute to tumour development. The pathway ... tensin homologue, PTEN. Endometrial carcinomas harbour frequent alterations in components of the pathway ...

    Abstract The phosphoinositide 3-kinase (PI3K) signalling pathway is highly dysregulated in cancer, leading to elevated PI3K signalling and altered cellular processes that contribute to tumour development. The pathway is normally orchestrated by class I PI3K enzymes and negatively regulated by the phosphatase and tensin homologue, PTEN. Endometrial carcinomas harbour frequent alterations in components of the pathway, including changes in gene copy number and mutations, in particular in the oncogene
    MeSH term(s) Animals ; Class I Phosphatidylinositol 3-Kinases/genetics ; Class I Phosphatidylinositol 3-Kinases/metabolism ; Endometrial Neoplasms/enzymology ; Endometrial Neoplasms/genetics ; Endometrial Neoplasms/metabolism ; Female ; Humans ; PTEN Phosphohydrolase/genetics ; PTEN Phosphohydrolase/metabolism ; Phosphatidylinositol 3-Kinase/genetics ; Phosphatidylinositol 3-Kinase/metabolism
    Chemical Substances Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; PTEN Phosphohydrolase (EC 3.1.3.67)
    Language English
    Publishing date 2018-12-07
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms19123931
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Catestatin induces glycogenesis by stimulating the phosphoinositide 3-kinase-AKT pathway.

    Bandyopadhyay, Gautam / Tang, Kechun / Webster, Nicholas J G / van den Bogaart, Geert / Mahata, Sushil K

    Acta physiologica (Oxford, England)

    2022  Volume 235, Issue 1, Page(s) e13775

    Abstract: ... dependent kinase-1 (PDK-1), GYS2, glycogen synthase kinase-3β (GSK-3β), AKT (a kinase in AKR mouse ... that produces Thymoma)/PKB (protein kinase B) and mammalian/mechanistic target of rapamycin (mTOR ... synthesis from UDPG, (c) reducing glycogenolysis and (d) enhancing downstream insulin signalling. ...

    Abstract Aim: Defects in hepatic glycogen synthesis contribute to post-prandial hyperglycaemia in type 2 diabetic patients. Chromogranin A (CgA) peptide Catestatin (CST: hCgA
    Methods: We determined liver glycogen, glucose-6-phosphate (G6P), uridine diphosphate glucose (UDPG) and glycogen synthase (GYS2) activities; plasma insulin, glucagon, noradrenaline and adrenaline levels in wild-type (WT) as well as in CST knockout (CST-KO) mice; glycogen synthesis and glycogenolysis in primary hepatocytes. We also analysed phosphorylation signals of insulin receptor (IR), insulin receptor substrate-1 (IRS-1), phosphatidylinositol-dependent kinase-1 (PDK-1), GYS2, glycogen synthase kinase-3β (GSK-3β), AKT (a kinase in AKR mouse that produces Thymoma)/PKB (protein kinase B) and mammalian/mechanistic target of rapamycin (mTOR) by immunoblotting.
    Results: CST stimulated glycogen accumulation in fed and fasted liver and in primary hepatocytes. CST reduced plasma noradrenaline and adrenaline levels. CST also directly stimulated glycogenesis and inhibited noradrenaline and adrenaline-induced glycogenolysis in hepatocytes. In addition, CST elevated the levels of UDPG and increased GYS2 activity. CST-KO mice had decreased liver glycogen that was restored by treatment with CST, reinforcing the crucial role of CST in hepatic glycogenesis. CST improved insulin signals downstream of IR and IRS-1 by enhancing phospho-AKT signals through the stimulation of PDK-1 and mTORC2 (mTOR Complex 2, rapamycin-insensitive complex) activities.
    Conclusions: CST directly promotes the glycogenic pathway by (a) reducing glucose production, (b) increasing glycogen synthesis from UDPG, (c) reducing glycogenolysis and (d) enhancing downstream insulin signalling.
    MeSH term(s) Animals ; Chromogranin A/pharmacology ; Epinephrine/pharmacology ; Glucose/metabolism ; Glycogen ; Glycogen Synthase Kinase 3 beta ; Humans ; Insulin/metabolism ; Liver Glycogen ; Mammals ; Mice ; Norepinephrine ; Peptide Fragments ; Phosphatidylinositol 3-Kinase ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Sirolimus ; TOR Serine-Threonine Kinases ; Uridine Diphosphate Glucose
    Chemical Substances Chromogranin A ; Insulin ; Liver Glycogen ; Peptide Fragments ; chromogranin A (344-364) ; Glycogen (9005-79-2) ; Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Glucose (IY9XDZ35W2) ; Uridine Diphosphate Glucose (V50K1D7P4Y) ; Sirolimus (W36ZG6FT64) ; Norepinephrine (X4W3ENH1CV) ; Epinephrine (YKH834O4BH)
    Language English
    Publishing date 2022-02-04
    Publishing country England
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2218636-0
    ISSN 1748-1716 ; 1748-1708
    ISSN (online) 1748-1716
    ISSN 1748-1708
    DOI 10.1111/apha.13775
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Novel roles for class II Phosphoinositide 3-Kinase C2β in signalling pathways involved in prostate cancer cell invasion.

    Mavrommati, Ioanna / Cisse, Ouma / Falasca, Marco / Maffucci, Tania

    Scientific reports

    2016  Volume 6, Page(s) 23277

    Abstract: Phosphoinositide 3-kinases (PI3Ks) regulate several cellular functions ... to other PI3Ks, there is still a limited understanding of the signalling pathways that can be specifically ... of the transcription factor Slug. These data identify novel signalling pathways specifically regulated by PI3K-C2β and ...

    Abstract Phosphoinositide 3-kinases (PI3Ks) regulate several cellular functions such as proliferation, growth, survival and migration. The eight PI3K isoforms are grouped into three classes and the three enzymes belonging to the class II subfamily (PI3K-C2α, β and γ) are the least investigated amongst all PI3Ks. Interest on these isoforms has been recently fuelled by the identification of specific physiological roles for class II PI3Ks and by accumulating evidence indicating their involvement in human diseases. While it is now established that these isoforms can regulate distinct cellular functions compared to other PI3Ks, there is still a limited understanding of the signalling pathways that can be specifically regulated by class II PI3Ks. Here we show that PI3K-C2β regulates mitogen-activated protein kinase kinase (MEK1/2) and extracellular signal-regulated kinase (ERK1/2) activation in prostate cancer (PCa) cells. We further demonstrate that MEK/ERK and PI3K-C2β are required for PCa cell invasion but not proliferation. In addition we show that PI3K-C2β but not MEK/ERK regulates PCa cell migration as well as expression of the transcription factor Slug. These data identify novel signalling pathways specifically regulated by PI3K-C2β and they further identify this enzyme as a key regulator of PCa cell migration and invasion.
    MeSH term(s) Butadienes/pharmacology ; Cell Line, Tumor ; Cell Movement/drug effects ; Down-Regulation ; Epidermal Growth Factor/pharmacology ; Humans ; MAP Kinase Kinase 1/metabolism ; MAP Kinase Kinase 2/metabolism ; Male ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Nitriles/pharmacology ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphoinositide-3 Kinase Inhibitors ; Phosphorylation/drug effects ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Protein Isoforms/antagonists & inhibitors ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; RNA Interference ; RNA, Small Interfering/metabolism ; Signal Transduction/drug effects ; Snail Family Transcription Factors/metabolism
    Chemical Substances Butadienes ; Nitriles ; Phosphoinositide-3 Kinase Inhibitors ; Protein Isoforms ; RNA, Small Interfering ; SNAI1 protein, human ; Snail Family Transcription Factors ; U 0126 ; Epidermal Growth Factor (62229-50-9) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24) ; MAP Kinase Kinase 1 (EC 2.7.12.2) ; MAP Kinase Kinase 2 (EC 2.7.12.2)
    Language English
    Publishing date 2016-03-17
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/srep23277
    Database MEDical Literature Analysis and Retrieval System OnLINE

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