<i>Connexin43</i> pseudogene in breast cancer cells offers a novel therapeutic target

Bier, Andrew; Oviedo-Landaverde, Irene; Zhao, Jing; Mamane, Yaël; Kandouz, Mustapha; Batist, Gerald

doi:10.1158/1535-7163.mct-08-0930

Cited by 46 publications

(35 citation statements)

References 47 publications

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“…Cx43 pseudogene has also been identified and implicated in breast cancer [81]. Pseudogenes are generally deemed nonfunctional copies of DNA.…”

Section: Connexin and Other Signaling Pathwaysmentioning

confidence: 99%

Connexin’s Connection in Breast Cancer Growth and Progression

Banerjee

2016

International Journal of Cell Biology

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Gap junctions are cell-to-cell junctions that are located in the basolateral surface of two adjoining cells. A gap junction channel is composed of a family of proteins called connexins. Gap junction channels maintain intercellular communication between two cells through the exchange of ions, small metabolites, and electrical signals. Gap junction channels or connexins are widespread in terms of their expression and function in maintaining the development, differentiation, and homeostasis of vertebrate tissues. Gap junction connexins play a major role in maintaining intercellular communication among different cell types of normal mammary gland for proper development and homeostasis. Connexins have also been implicated in the pathogenesis of breast cancer. Differential expression pattern of connexins and their gap junction dependent or independent functions provide pivotal cross talk of breast tumor cells with the surrounding stromal cell in the microenvironment. Substantial research from the last 20 years has accumulated ample evidences that allow us a better understanding of the roles that connexins play in the tumorigenesis of primary breast tumor and its metastatic progression. This review will summarize the knowledge about the connexins and gap junction activities in breast cancer highlighting the differential expression and functional dynamics of connexins in the pathogenesis of the disease.

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“…Cx43 pseudogene has also been identified and implicated in breast cancer [81]. Pseudogenes are generally deemed nonfunctional copies of DNA.…”

Section: Connexin and Other Signaling Pathwaysmentioning

confidence: 99%

Connexin’s Connection in Breast Cancer Growth and Progression

Banerjee

2016

International Journal of Cell Biology

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“…To further assess the role of GJIC in cell density-dependent adriamycin sensitivity, siRNA was used to downregulate the expression of Cx43 in these cells (27,28). Downregulation was achieved by transient transfection of Hs578T and MCF-7 cells with synthetic Cx43-targeted siRNA.…”

Section: Influence Of Sirna On Cx43 Expression and Function Of Gjmentioning

confidence: 99%

Influence of gap junction intercellular communication composed of connexin 43 on the antineoplastic effect of adriamycin in breast cancer cells

Jiang

Dong

et al. 2016

Oncology Letters

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Abstract. Gap junctions (GJs) serve the principal role in the antineoplastic (cytotoxicity and induced apoptosis) effect of chemical drugs. The aim of the present study was to determine the effect of GJ intercellular communication (GJIC) composed of connexin 43 (Cx43) on adriamycin cytotoxicity in breast cancer cells. Four cell lines (Hs578T, MCF-7, MDA-MB-231 and SK-BR-3) with different degree of malignancy were used in the study. The results of western blotting and immunofluorescence revealed that, in Hs578T and MCF-7 cells, which have a low degree of malignancy, the expression levels of Cx43 and GJIC were higher than those in MDA-MB-231 and SK-BR-3 cells (which have a high degree of malignancy). In Hs578T and MCF-7 cells, where GJ could be formed, the function of GJ was modulated by a pharmacological potentiators [retinoid acid (RA)]/inhibitors [oleamide and 18-α-glycyrrhetinic acid (18-α-GA)] and small interfering RNA (siRNA). In high-density cells (where GJ was formed), enhancement of GJ function by RA increased the cytotoxicity of adriamycin, while inhibition of GJ function by oleamide/18-α-GA and siRNA decreased the cytotoxicity caused by adriamycin. Notably, the modulation of GJ did not affect the survival of cells treated with adriamycin when cells were in low density (no GJ was formed). The present study illustrated the association between GJIC and the antitumor effect of adriamycin in breast cancer cells. The cytotoxicity of adriamycin on breast cancer cells was increased when the function of gap junctions was enhanced.

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“…Similarly, a pseudogene of Connexin 43 ( PsiCx43 ) was found to be expressed in breast cancer cells, but not in normal cells. Inhibition of PsiCx43 resulted in an increase in Connexin 43 expression and sensitized cells to cytotoxic chemotherapy [49]. Pseudogenes of BRAF were expressed in thyroid cancers, where they activate the MAPK pathway and promote oncogenic transformation [50].…”

Section: Pseudogene Functionsmentioning

confidence: 99%

Not so Pseudo Anymore: Pseudogenes as Therapeutic Targets

Roberts

Morris

2013

Pharmacogenomics

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Pseudogenes are junk DNA gene remnants generated by inactivating mutations or the loss of regulatory sequences, often following gene duplication or retrotransposition events. These pseudogenes have previously been considered to be molecular fossils derived from once-coding genes. In many cases, pseudogenes confer no observable selective advantage to the host organism and may be on a path towards removal from the genome. However, pseudogenes can also serve as raw material for the exaptation of novel functions, particularly in relation to the regulation of gene expression. Many pseudogenes are resurrected as noncoding RNA genes, which function in RNA-based gene regulatory circuits. As such, functional pseudogenes might simply be considered as ‘genes’. Here, we discuss the role of these pseudogene-derived RNAs as regulators of gene expression in the context of human disease. In particular, we consider the manipulation of pseudogene transcripts through the use of antisense oligonucleotides, siRNAs, aptamers or classical gene therapy approaches as novel pharmacological strategies.

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Connexin43 pseudogene in breast cancer cells offers a novel therapeutic target

Cited by 46 publications

References 47 publications

Connexin’s Connection in Breast Cancer Growth and Progression

Connexin’s Connection in Breast Cancer Growth and Progression

Influence of gap junction intercellular communication composed of connexin 43 on the antineoplastic effect of adriamycin in breast cancer cells

Not so Pseudo Anymore: Pseudogenes as Therapeutic Targets

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