Gap junctional communication in cultured human lung carcinoma cells

Tomai, Evangelia; Brownell, Heather L.; Tufescu, Ted; Kenneth, Reid; Campling, Barbara G.; Raptis, Leda

doi:10.1016/s0169-5002(99)00016-1

Cited by 21 publications

(21 citation statements)

References 32 publications

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“…In light of the above findings, we examined GJIC levels at different densities up to 4 days post-confluence in a panel of human lung cancer lines [18]. Two NSCLC lines, QU-DB (Figure 2A, a-c ) and SK-LuCi6 (Table 1,A) displayed extensive GJIC at their peak density, while five NSCLC lines had very low GJIC (e.g.…”

Section: Resultsmentioning

confidence: 99%

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Stat3 is a positive regulator of gap junctional intercellular communication in cultured, human lung carcinoma cells

et al. 2012

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BackgroundNeoplastic transformation of cultured cells by a number of oncogenes such as src suppresses gap junctional, intercellular communication (GJIC); however, the role of Src and its effector Signal transducer and activator of transcription-3 (Stat3) upon GJIC in non small cell lung cancer (NSCLC) has not been defined. Immunohistochemical analysis revealed high Src activity in NSCLC biopsy samples compared to normal tissues. Here we explored the potential effect of Src and Stat3 upon GJIC, by assessing the levels of tyr418-phosphorylated Src and tyr705-phosphorylated Stat3, respectively, in a panel of NSCLC cell lines.MethodsGap junctional communication was examined by electroporating the fluorescent dye Lucifer yellow into cells grown on a transparent electrode, followed by observation of the migration of the dye to the adjacent, non-electroporated cells under fluorescence illumination.ResultsAn inverse relationship between Src activity levels and GJIC was noted; in five lines with high Src activity GJIC was absent, while two lines with extensive GJIC (QU-DB and SK-LuCi6) had low Src levels, similar to a non-transformed, immortalised lung epithelial cell line. Interestingly, examination of the mechanism indicated that Stat3 inhibition in any of the NSCLC lines expressing high endogenous Src activity levels, or in cells where Src was exogenously transduced, did not restore GJIC. On the contrary, Stat3 downregulation in immortalised lung epithelial cells or in the NSCLC lines displaying extensive GJIC actually suppressed junctional permeability.ConclusionsOur findings demonstrate that although Stat3 is generally growth promoting and in an activated form it can act as an oncogene, it is actually required for gap junctional communication both in nontransformed lung epithelial cells and in certain lung cancer lines that retain extensive GJIC.

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Section: Resultsmentioning

confidence: 99%

“…We previously assessed GJIC in a number of lung cancer lines [18]. In the present work GJIC was examined using an apparatus where cells were grown on a glass slide, half of which was coated with electrically conductive, optically transparent, indium-tin oxide.…”

Section: Introductionmentioning

confidence: 99%

Stat3 is a positive regulator of gap junctional intercellular communication in cultured, human lung carcinoma cells

et al. 2012

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“…Cells are grown and electroporated on a glass slide (1), coated with conductive and transparent ITO (1a) with a surface resistivity of 20 O=square (Colorado Concept Coatings, Loveland, CO) (Tomai et al, 1998). The ITO was etched to define electrode and nonconducting regions, which were electrically isolated from each other by removing the ITO coating in lines of *20 mm wide from the glass surface.…”

Section: Examination Of Gap Junctional Communicationmentioning

confidence: 99%

Stat3 Activity Is Required for Gap Junctional Permeability in Normal Rat Liver Epithelial Cells

Geletu

Chaize

Arulanandam

et al. 2009

DNA and Cell Biology

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Neoplastic transformation by oncogenes such as activated Src is known to suppress gap junctional, intercellular communication (GJIC). One of the Src effector pathways leading to GJIC suppression and transformation is the Ras/Raf/Mek/Erk, so that inhibition of this pathway in vSrc-transformed cells restores GJIC. A distinct Src downstream effector required for neoplasia is the signal transducer and activator of transcription-3 (Stat3). To examine the role of Stat3 upon the Src-mediated, GJIC suppression, Stat3 was downregulated in rat liver epithelial cells expressing activated Src through treatment with the CPA7, Stat3 inhibitor, or through infection with a retroviral vector expressing a Stat3-specific shRNA. GJIC was examined by electroporating the fluorescent dye, Lucifer yellow, into cells grown on two coplanar electrodes of electrically conductive, optically transparent, indium-tin oxide, followed by observation of the migration of the dye to the adjacent, nonelectroporated cells under fluorescence illumination. The results demonstrate that, contrary to inhibition of the Ras pathway, Stat3 inhibition in cells expressing activated Src does not restore GJIC. On the contrary, Stat3 inhibition in normal cells with high GJIC levels eliminated junctional permeability. Therefore, Stat3's function is actually required for the maintenance of junctional permeability, although Stat3 generally promotes growth and in an activated form can act as an oncogene.

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“…were shifted into tumor cells, could inhibit the tumor growth and up-regulate the gap junction intercellular communication so as to recover the normal growth of tumor cells (Tomai et al, 1999;Yamasaki et al, 1999;McLachlan et al, 2006;Hattori et al, 2007;Langlois et al, 2010). These indicated that connexin genes were a family of tumor suppressor genes (Plante et al, 2011;Ogawa et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Expression of Connexin 43 and E-cadherin Protein and mRNA in Non-small Cell Lung Cancers in Chinese Patients

Zhao

Sun²,

Liu³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Gap junctional communication in cultured human lung carcinoma cells

Cited by 21 publications

References 32 publications

Stat3 is a positive regulator of gap junctional intercellular communication in cultured, human lung carcinoma cells

Stat3 is a positive regulator of gap junctional intercellular communication in cultured, human lung carcinoma cells

Stat3 Activity Is Required for Gap Junctional Permeability in Normal Rat Liver Epithelial Cells

Expression of Connexin 43 and E-cadherin Protein and mRNA in Non-small Cell Lung Cancers in Chinese Patients

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