Connexin 43 mediated gap junctional communication enhances breast tumor cell diapedesis in culture

Pollmann, Mary-Ann; Shao, Qing; Laird, Dale W.; Sandig, Martin

doi:10.1186/bcr1042

Cited by 103 publications

(106 citation statements)

References 63 publications

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“…A similar effect was previously demonstrated for normal HEk-293 cell populations, where GJIC inhibited by organotin compounds was partially restored by NAC (24). High levels of connexin expression and GJIC often correlate with a single cancer cell invasive potential indicating that connexins (7,22) and gap junctional coupling (8,23) are crucial for cancer progression. we suggest the existence of a common system which regulates cancer cell motility and gap junctional coupling in prostate cancer cell populations.…”

Section: Discussionsupporting

confidence: 58%

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Fenofibrate attenuates contact-stimulated cell motility and gap junctional coupling in DU-145 human prostate cancer cell populations

Madeja

2011

Oncol Rep

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Abstract. In the present study, we investigated the effects of fenofibrate on the invasive potential of DU-145 human prostate cancer cells in the context of gap junctional intercellular coupling and the formation of reactive oxygen species. Timelapse analyses of cell motility, accompanied by tests of cell viability, membrane microviscosity, reactive oxygen species accumulation and the function of gap junctional protein connexin 43 were performed in monolayer cultures of DU-145 cells following fenofibrate administration. Fenofibrate inhibited the motility of DU-145 cells and attenuated gap junctional intercellular coupling in a manner independent of its effects on cell viability, PPARα activation and cell membrane microviscosity. Instead, N-acetyl-L-cysteine, a scavenger of reactive oxygen species, restored cell motility and gap junctional coupling in fenofibrate-treated DU-145 cell populations. These data indicate that two parameters crucial for cancer cell metastatic potential, i.e. cell motility and gap junctional coupling, are inhibited by fenofibrate. Thus, fenofibrate affects prostate cancer cell invasion via an orchestrated action on versatile cancer cell properties determining this process. A novel mechanism of anti-invasive activity of fenofibrate, which depends on its interference with cell motility and the function of gap junctions regulated by reactive oxygen species, is suggested.

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Section: Discussionsupporting

confidence: 58%

“…In particular, deregulation of GJIC facilitates early carcinogenesis and the formation of a local hyperplasia (2)(3)(4)(5). In contrast, restoration of GJIC between cancer and normal cells is crucial for malignant cell dissemination (6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

Fenofibrate attenuates contact-stimulated cell motility and gap junctional coupling in DU-145 human prostate cancer cell populations

Madeja

2011

Oncol Rep

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“…The inhibition of Calcein transference observed in the presence of a connexin inhibitor and in Cx43-knockdown osteosarcoma cells confirmed the key role played by the Cx43 in GJIC process (Aftab et al, 2015). Our assessment of functional GJIC in HOS cells done by DEPArrayª microfluidic approach is in agreement with a recent new high throughput screening proposed by Lee et al (2015) between the two cell types during this crucial phase (Pollmann et al, 2005, Saito-Katsuragi et al 2007). In line with several studies (Gramsch et al 2001, Matemba et al 2006, we found an increase in Cx43 expression in the differentiated osteoblasts.…”

Section: Osteosarcoma Cells Transduced Withsupporting

confidence: 88%

Analysis of gap junctional intercellular communications using a dielectrophoresis-based microchip

Gabriel

Charrier

Royer

et al. 2017

European Journal of Cell Biology

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International audiencePlease cite this article in press as: Tellez-Gabriel, M., et al., Analysis of gap junctional intercellular communications using a dielectrophoresis-based microchip. Gap junctions are transmembrane structures that directly connect the cytoplasm of adjacent cells, making intercellular communications possible. It has been shown that the behaviour of several tumours – such as bone tumours – is related to gap junction intercellular communications (GJIC). Several methodologies are available for studying GJIC, based on measuring different parameters that are useful for multiple applications, such as the study of carcinogenesis for example. These methods nevertheless have several limitations. The present manuscript describes the setting up of a dielectrophoresis (DEP)-based lab-on-a-chip platform for the real-time study of Gap Junctional Intercellular Communication between osteosarcoma cells and the main cells accessible to their microenvironment. We conclude that using the DEParray technology for the GJIC assessment has several advantages comparing to current techniques. This methodology is less harmful for cells integrity; cells can be recovered after interaction to make further molecular analysis; it is possible to study GJIC in real time; we can promote cell interactions using up to five different populations. The setting up of this new methodology overcomes several difficulties to perform experiments for solving questions about GJIC process that we are not able to do with current technics

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“…On the other hand, connexins can enhance the invasive potential of cancer cells in a GJIC-dependent as well as GJICindependent manner [13][14][15]. While GJIC between cancer and endothelial cells was shown to facilitate cancer cell penetration of the endothelial layer [16,17], a GJIC-independent function of Cx43 in brain tumour invasion was reported [14]. These observations suggest the stage-specific function of connexins in the process of cancer development [15].…”

Section: Introductionmentioning

confidence: 90%

DU-145 prostate carcinoma cells that selectively transmigrate narrow obstacles express elevated levels of Cx43

Szpak

Wybieralska

Niedzialkowska

et al. 2011

Cellular and Molecular Biology Letters

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The formation of aqueous intercellular channels mediating gap junctional intercellular coupling (GJIC) is a canonical function of connexins (Cx). In contrast, mechanisms of GJIC-independent involvement of connexins in cancer formation and metastasis remain a matter of debate. Because of the role of Cx43 in the determination of carcinoma cell invasive potential, we addressed the problem of the possible Cx43 involvement in early prostate cancer invasion. For this purpose, we analysed Cx43-positive DU-145 cell subsets established from the progenies of the cells most readily transmigrating microporous membranes. These progenies displayed motile activity similar to the control DU-145 cells but were characterized by elevated Cx43 expression levels and GJIC intensity. Thus, apparent links exist between Cx43 expression and transmigration potential of DU-145 cells. Moreover, Cx43 expression profiles in the analysed DU-145 subsets were not affected by intercellular contacts and chemical inhibition of GJIC during the transmigration. Our observations indicate that neither cell motility nor GJIC determines the transmigration efficiency of DU-145 cells. However, we postulate that selective transmigration of prostate cancer cells expressing elevated levels of Cx43 expression may be crucial for the “leading front” formation during cancer invasion.

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Connexin 43 mediated gap junctional communication enhances breast tumor cell diapedesis in culture

Cited by 103 publications

References 63 publications

Fenofibrate attenuates contact-stimulated cell motility and gap junctional coupling in DU-145 human prostate cancer cell populations

Fenofibrate attenuates contact-stimulated cell motility and gap junctional coupling in DU-145 human prostate cancer cell populations

Analysis of gap junctional intercellular communications using a dielectrophoresis-based microchip

DU-145 prostate carcinoma cells that selectively transmigrate narrow obstacles express elevated levels of Cx43

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