Contact stimulation of prostate cancer cell migration: the role of gap junctional coupling and migration stimulated by heterotypic cell-to-cell contacts in determination of the metastatic phenotype of Dunning rat prostate cancer cells

Bursting in inhibitory interneuronal networks: a role for gap-junctional coupling. Much work now emphasizes the concept that interneuronal networks play critical roles in generating synchronized, oscillatory behavior. Experimental work has shown that functional inhibitory networks alone can produce synchronized activity, and theoretical work has demonstrated how synchrony could occur in mutually inhibitory networks. Even though gap junctions are known to exist between interneurons, their role is far from clear. We present a mechanism by which synchronized bursting can be produced in a minimal network of mutually inhibitory and gap-junctionally coupled neurons. The bursting relies on the presence of persistent sodium and slowly inactivating potassium currents in the individual neurons. Both GABAA inhibitory currents and gap-junctional coupling are required for stable bursting behavior to be obtained. Typically, the role of gap-junctional coupling is focused on synchronization mechanisms. However, these results suggest that a possible role of gap-junctional coupling may lie in the generation and stabilization of bursting oscillatory behavior.

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Role of C17orf37/MGC14832 in prostate cancer cell proliferation and migration

The FASEB Journal ◽

10.1096/fasebj.21.5.a289-b ◽

2007 ◽

Vol 21 (5) ◽

Author(s):

Subhamoy Dasgupta ◽

Jamboor K Vishwanatha

Keyword(s):

Prostate Cancer ◽

Cell Proliferation ◽

Cancer Cell ◽

Prostate Cancer Cell ◽

Cancer Cell Proliferation ◽

Cell Proliferation And Migration ◽

And Migration ◽

Proliferation And Migration

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The stage-specific function of gap junctions during tumourigenesis

Cellular & Molecular Biology Letters ◽

10.2478/s11658-007-0039-5 ◽

2008 ◽

Vol 13 (1) ◽

Cited By ~ 42

Author(s):

Jarosław Czyż

Keyword(s):

Gap Junctions ◽

Surrounding Tissue ◽

Metastatic Tumour ◽

Connexin Expression ◽

Cell Parameters ◽

Tumour Promotion ◽

Junctional Coupling ◽

Gap Junctional ◽

Gap Junctional Coupling

AbstractTumour development is a process resulting from the disturbance of various cellular functions including cell proliferation, adhesion and motility. While the role of these cell parameters in tumour promotion and progression has been widely recognized, the mechanisms that influence gap junctional coupling during tumorigenesis remain elusive. Neoplastic cells usually display decreased levels of connexin expression and/or gap junctional coupling. Thus, impaired intercellular communication via gap junctions may facilitate the release of a potentially neoplastic cell from the controlling regime of the surrounding tissue, leading to tumour promotion. However, recent data indicates that metastatic tumour cell lines are often characterized by relatively high levels of connexin expression and gap junctional coupling. This review outlines current knowledge on the role of connexins in tumorigenesis and the possible mechanisms of the interference of gap junctional coupling with the processes of tumour invasion and metastasis.

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Inhibition of cancer cell-derived exosomal microRNA-183 suppresses cell growth and metastasis in prostate cancer by upregulating TPM1

Cancer Cell International ◽

10.1186/s12935-020-01686-x ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Yanping Dai ◽

Xiaoqin Gao

Keyword(s):

Prostate Cancer ◽

Cell Proliferation ◽

Cancer Cell ◽

Prostate Cancer Cell ◽

Expression Patterns ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Invasion And Migration ◽

And Migration

Abstract Background Emerging evidence continues to highlight the significant role of microRNAs (miRNAs) in the regulation of cancer growth and metastasis. Herein, the current study aimed to elucidate the role of exosomal miR-183 in prostate cancer development. Methods Initially, public microarray-based gene expression profiling of prostate cancer was employed to identify differentially expressed miRNAs. The putative target gene TPM1 of miR-183 was subsequently predicted, followed by the application of a luciferase reporter assay and examination of the expression patterns in prostate cancer patients and cell lines. The effects of miR-183 and TPM1 on processes such as cell proliferation, invasion and migration were evaluated using in vitro gain- and loss-of-function experiments. The effect of PC3 cells-derived exosomal miR-183 was validated in LNCaP cells. In vivo experiments were also performed to examine the effect of miR-183 on prostate tumor growth. Results High expression of miR-183 accompanied with low expression of TPM1 was detected in prostate cancer. Our data indicated that miR-183 could target and downregulate TPM1, with the overexpression of miR-183 and exosomal miR-183 found to promote cell proliferation, migration, and invasion in prostate cancer. Furthermore, the tumor-promoting effect of exosome-mediated delivery of miR-183 was subsequently confirmed in a tumor xenograft model. Conclusions Taken together, the key findings of our study demonstrate that prostate cancer cell-derived exosomal miR-183 enhance prostate cancer cell proliferation, invasion and migration via the downregulation of TPM1, highlighting a promising therapeutic target against prostate cancer.

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Increasing Gap Junctional Coupling: A Tool for Dissecting the Role of Gap Junctions

The Journal of Membrane Biology ◽

10.1007/s00232-007-9026-z ◽

2007 ◽

Vol 216 (1) ◽

pp. 23-35 ◽

Cited By ~ 14

Author(s):

Lene Nygaard Axelsen ◽

Ketil Haugan ◽

Martin Stahlhut ◽

Anne-Louise Kjølbye ◽

James K. Hennan ◽

...

Keyword(s):

Gap Junctions ◽

Junctional Coupling ◽

Gap Junctional ◽

Gap Junctional Coupling

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Connexins and steroidogenesis in mouse Leydig cells

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2012-0385 ◽

2013 ◽

Vol 91 (2) ◽

pp. 157-164 ◽

Cited By ~ 11

Author(s):

Dan Li ◽

Poonampreet Sekhon ◽

Kevin J. Barr ◽

Lucrecia Márquez-Rosado ◽

Paul D. Lampe ◽

...

Keyword(s):

Gap Junctions ◽

Leydig Cell ◽

Leydig Cells ◽

Adult Mouse ◽

Chain Reaction ◽

Junctional Coupling ◽

Polymerase Chain ◽

Gap Junctional ◽

Gap Junctional Coupling

Connexin43 has been recognized as forming gap junctions in Leydig cells. However, previous work has shown that mouse Leydig cells lacking this connexin do not suffer any limitation of their ability to produce testosterone when stimulated with luteinizing hormone. The objective of this study was to identify additional connexins in mouse Leydig cells that could be required for steroidogenesis. A reverse transcription – polymerase chain reaction screen involving isolated adult Leydig cells identified connexin36 and connexin45 as expressed along with connexin43. Treatment of dissociated testes with carbenoxolone, a nonspecific blocker of gap junctional coupling, significantly reduced testosterone output as did treatment with quinine, which disrupts coupling provided by connexin36 and connexin45 gap junctions but not those composed of connexin43, indicating that either or both of connexins 36 and 45 could be involved in supporting Leydig cell steroidogenesis. Immunolabeling of adult mouse testis sections confirmed the localization of connexin36 along with connexin43 in Leydig cell gap junctions but not connexin45, which is distributed throughout the cells. It was concluded that connexin36, connexin43, and connexin45 are coexpressed in Leydig cells with connexins 36 and 43 contributing to gap junctions. The role of connexin45 remains to be elucidated.

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Apigenin inhibits growth and motility but increases gap junctional coupling intensity in rat prostate carcinoma (MAT-LyLu) cell populations

Cellular & Molecular Biology Letters ◽

10.2478/s11658-008-0003-z ◽

2008 ◽

Vol 13 (3) ◽

Cited By ~ 9

Author(s):

Marta Czernik ◽

Jolanta Sroka ◽

Zbigniew Madeja ◽

Jarosław Czyż

Keyword(s):

Cell Proliferation ◽

Cell Motility ◽

Cell Model ◽

Inhibitory Effect ◽

Cancer Development ◽

Junctional Coupling ◽

Rat Prostate ◽

Gap Junctional ◽

Gap Junctional Coupling

AbstractApigenin (4′,5,7,-trihydroxyflavone) is a flavonoid abundant in the common fruits, herbs and vegetables constituting the bulk of the human diet. This study was aimed at quantifying the effects of apigenin on the basic cellular traits determining cancer development, i.e. cell proliferation, gap junctional coupling, and motility, using the Dunning rat prostate MAT-LyLu cell model. We demonstrated that apigenin considerably inhibits MAT-LyLu cell proliferation and significantly enhances the intensity of connexin43-mediated gap junctional coupling. This effect correlates with an increased abundance of C×43-positive plaques at the cell-to-cell borders seen in apigenin-treated variants. Moreover, we observed an inhibitory effect of apigenin on the motility of MAT-LyLu cells. The basic parameters characterising MAT-LyLu cell motility, especially the rate of cell displacement, considerably decreased upon apigenin administration. This in vitro data indicates that apigenin may affect cancer development in general, and prostate carcinogenesis in particular, via its influence on cellular activities decisive for both cancer promotion and progression, including cell proliferation, gap junctional coupling and cell motility and invasiveness.

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