Loss of Pannexin 1 Attenuates Melanoma Progression by Reversion to a Melanocytic Phenotype

Peñuela, Silvia; Gyenis, Laszlo; Ablack, Amber; Churko, Jared M.; Berger, Amy; Litchfield, David W.; Lewis, John D.; Laird, Dale W.

doi:10.1074/jbc.m112.377176

Cited by 96 publications

(112 citation statements)

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“…The chick CAM avian embryo model has been widely used as a model for tumorigenesis in vivo, including the assessment of melanoma tumor growth and metastasis (26,31). We found that control melanomas produced relatively large tumors, not unlike tumors produced by Cx26-expressing melanomas.…”

Section: Discussionmentioning

confidence: 75%

“…In Vivo Chick Chorioallantoic Membrane (CAM) Assay-Primary tumor properties of BL6 cells in the chicken embryo was assessed as previously described (31). Briefly, fertilized chicken eggs (McKinley Hatchery, St. Mary's, Canada) were incubated in an automated rotary incubator (GQF Manufacturing Company) under 40% humidity at 37°C for 3 days, rotating once every hour.…”

Section: Methodsmentioning

confidence: 99%

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Connexin43 Reduces Melanoma Growth within a Keratinocyte Microenvironment and during Tumorigenesis in Vivo

Ableser

Peñuela

Lee

et al. 2014

Journal of Biological Chemistry

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Background: Cx43 is a gap junction protein that is highly expressed in the epidermis. Results: Ectopic expression of Cx43 in gap junctional intercellular communication-deficient melanomas reduces growth in keratinocyte co-cultures and tumorigenicity assays. Conclusion: Cx43 acts as a tumor suppressor during melanoma tumorigenesis. Significance: Cx43 may serve as a potential therapeutic target for melanomas.

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Section: Discussionmentioning

confidence: 75%

Section: Methodsmentioning

confidence: 99%

Connexin43 Reduces Melanoma Growth within a Keratinocyte Microenvironment and during Tumorigenesis in Vivo

Ableser

Peñuela

Lee

et al. 2014

Journal of Biological Chemistry

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“…In astrocytes, Connexin-43 is required for cell migration under pro-inflammatory conditions and it interacts with many cytoskeletal proteins, such as β-actin and glial fibrillary acidic protein [40,41]. Conversely, pannexins regulate motility of different cell types, such as neutrophils or leucocytes, tumor cells, venous fibroblasts, and neurons, among others [42][43][44]. Given these observations, we evaluated whether these hemichannels participate in Thy-1-induced migration of astrocytes by mediating ATP release and P2X7R activation.…”

Section: Accepted M Manuscriptmentioning

confidence: 99%

Integrin-mediated transactivation of P2X7R via hemichannel-dependent ATP release stimulates astrocyte migration

Álvarez

Lagos-Cabré

Kong

et al. 2016

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

109

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Leyton, Integrin-mediated transactivation of P2X7R via hemichannel-dependent ATP release stimulates astrocyte migration, BBA -Molecular Cell Research (2016Research ( ), doi: 10.1016Research ( /j.bbamcr.2016 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPT

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“…Furthermore, Panx-1-depleted B16 melanoma cells exhibit reduced cell migration and growth, resembling normal melanocytes. Knockdown of Panx-1 in mice also has the effect of reducing tumor size in vivo [8]. Moreover, Panx-1 is highly expressed in human platelets, and Panx-1 channels can promote the aggregation of platelets, which is a risk factor of cancer metastasis, by enhancing Ca 2+ influx and ATP release [9].…”

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confidence: 99%

“…These data supported that Panx-1 has a tumorsuppressor property, while some other studies indicated that Panx-1 promotes the development of cancer. Penuela et al [8] found that Panx-1 is upregulated in B16 melanoma cells rather than in normal melanocytes. Furthermore, Panx-1-depleted B16 melanoma cells exhibit reduced cell migration and growth, resembling normal melanocytes.…”

mentioning

confidence: 99%

A new perspective of mechanosensitive pannexin-1 channels in cancer metastasis: clues for the treatment of other stress-induced diseases

2016

ABBS

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Cancer metastasis is a process that cancer cells deviate from the primary site and spread to the other areas to form new colonies, which is the leading cause of death in cancer patients. During metastatic progression, circulating cancer cells lodge within the microvasculature of end organs, where most of them die from mechanical deformation. However, cancer cells can survive from mechanical deformation by unknown mechanisms. Recently, Furlow et al.[1] identified a mutation truncated form of pannexin-1 (Panx-1), PANX1 1-89 , which was significantly enriched in highly metastatic cancer cells. PANX1 augmented Panx-1 channel-mediated adenosine triphosphate (ATP) release and enhanced the efficiency of metastasis by promoting metastatic breast cancer cells survival during physical deformation. Additionally, carbenoxolone (CBX), a Panx-1 inhibitor, was proved to reduce the efficiency of breast cancer metastasis. These results suggested that Panx-1 is one of the molecular bases for metastatic cell survival in microvasculature-induced biomechanical trauma [1]. In 2000, three members of pannexins, including Panx-1, Panx-2, and Panx-3, have been found to be new members of gap-junctions' family [2]. Panx-1 was ubiquitously expressed in human tissues. Subsequent studies further revealed that Panx-1 forms single-pass membrane channels that connect the intracellular and extracellular compartments rather than forming intercellular channels spanning the two plasma membranes, which is mainly different from classical gap junctions [3]. Physiologically, Panx-1 channels are mainly involved in the efflux of ATP and regulate cellular inflammasomes [4]. Many studies indicated that Panx-1 is related to epilepsy, neuropathic pain, painful musculoskeletal diseases, ischemia injury, myocardial fibrosis, overactivity of the human bladder, and cancers [5][6][7][8][9][10][11][12][13] (Fig. 1 ).The beneficial or aggravating role of Panx-1 in cancer remains controversial. Lai et al. [5] reported that Panx-1 plays a tumor-suppressive role in vitro and in vivo. Reverse transcription polymerase chain reaction analysis revealed that C6 cells do not express Panx-1. However, stable expression of Panx-1 in C6 glioma cells significantly inhibits cell growth, proliferation, and motility in vitro [5]. Besides, Panx-1 is an important intratumor biomechanical environment regulator that accelerates the dynamic assembly of multicellular C6 glioma aggregates [6]. Panx-1 also significantly reduces the tumor size in athymic nude mice [5,6]. Derangere et al. [7] reported that caspase-1-dependent colon cancer cell pyroptosis is mainly induced through the interaction with Panx-1. These data supported that Panx-1 has a tumorsuppressor property, while some other studies indicated that Panx-1 promotes the development of cancer. Penuela et al. [8] found that Panx-1 is upregulated in B16 melanoma cells rather than in normal melanocytes. Furthermore, Panx-1-depleted B16 melanoma cells exhibit reduced cell migration and growth, resembling normal melanocytes. Knockdown o...

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Loss of Pannexin 1 Attenuates Melanoma Progression by Reversion to a Melanocytic Phenotype

Cited by 96 publications

References 44 publications

Connexin43 Reduces Melanoma Growth within a Keratinocyte Microenvironment and during Tumorigenesis in Vivo

Connexin43 Reduces Melanoma Growth within a Keratinocyte Microenvironment and during Tumorigenesis in Vivo

Integrin-mediated transactivation of P2X7R via hemichannel-dependent ATP release stimulates astrocyte migration

A new perspective of mechanosensitive pannexin-1 channels in cancer metastasis: clues for the treatment of other stress-induced diseases

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