Rat gap junction connexin-30 inhibits proliferation of glioma cell lines

Abstract

Connexins, the structural components of gap junctions, control cell growth and differentiation and are believed to belong to a family of tumour suppressor genes. Studies on connexin localization in brain showed that several of these proteins were expressed in distinct compartments of the brain in a cell-type specific manner, indicating that different gap junctions play specific roles in the physiology of the mammalian brain. In this report, we first cloned rat connexin-30 cDNA from brain and showed that it was expressed in long-term primary culture of rat astrocytes. In order to examine the potential role of connexin-30 in tumour cell proliferation, we transfected the connexin-30 cDNA into two rat glioma cell lines (9L and C6) which have lost its expression. Transfected clones adequately expressed membrane-bound connexin-30 protein. Connexin-30-expressing clones showed slower growth, lower DNA synthesis and reduced proliferation in soft agar as compared with the parental and control cells. We concluded that connexin-30 may also probably be considered as a tumour suppressor in rat gliomas.

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

“…Here, we show that Cx43 expression in Cx-deficient melanomas reduces the total cell number via delayed passage through the S phase of the cell cycle. Likewise, the expression of Cx26 in cancer cells has also been reported to reduce cell proliferation (34), as has the related and often co-expressed Cx30 isoform (42). However, here we found that Cx26 exhibited no significant effect on cell proliferation in melanomas, suggesting tumor cell specific differences.…”

Identification of stage-specific biomarkers in lung adenocarcinoma based on RNA-seq data

“…Intriguingly, the expression of GJB6 was increased in the stage II of LAC, suggesting that GJB6 serves as an enhancer in the proliferation of tumor cells [35], which may be involved in the LAC pathogenesis by disrupting intercellular communication. However, inconsistent results are reported in previous studies indicating that its role in tumorigenesis remains to be defined [36,37].…”

Connexin-related signaling in cell death: to live or let die?

“…In most cases, the evidence is based on experiments in which Cx expression was artificially modified (Table 1). Cx overexpression was found to trigger cell cycle arrest [168][169][170][171][172][173] and cellular differentiation 174 without influencing Cx channel activity in any way. In a similar manner, transfection of C6 rat glioma cells with Cx43, Cx40 or Cx32 genes resulted in an increased resistance to exogenously induced cellular injury, independently of GJIC.…”