Aberrant expression and localization of connexin43 and connexin30 in a rat glioma cell line.

Abstract:

:Gap junctions are cellular structures which permit direct exchanges of small molecules from cytoplasm to cytoplasm in most of the cells of metazoan organisms. For four decades, it has been observed that the inhibition of this type of intercellular communication is often associated with tumorigenesis. The assumption that loss of homeostasis which characterizes tumor growth could be a consequence of a lack of gap junctional intercellular communication (GJIC) has been reinforced by strategies able to reinduce both GJIC and normalization of the phenotype. So far, no molecular data may explain clearly how gap junctions can regulate cell proliferation. It has been argued that the gap-junction tumor suppressive effect may depend specifically on the connexin type which is expressed. For instance, the transfection of connexin30 (Cx30), a gap junction protein, has been previously associated with a slower growth of rat glioma cells (9L cells). Here, we show that these cells do communicate less compared to the Cx43-expressing parental cells even if the Cx30-transfected cells do express more Cx43. This result was related to the cytoplasmic distribution of Cx43 and a nuclear localization of both the Cx30 and a 20-kDa fragment corresponding to a Cx43 signal. According to these data, it seems that cell growth regulation may depend more on the behavior of connexins than the simple establishment of GJIC.

journal_name

Mol Carcinog

journal_title

Molecular carcinogenesis

authors

Mennecier G,Derangeon M,Coronas V,Hervé JC,Mesnil M

doi

10.1002/mc.20393

subject

Has Abstract

pub_date

2008-05-01 00:00:00

pages

391-401

issue

5

eissn

0899-1987

issn

1098-2744

journal_volume

47

pub_type

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