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Disrupted traffic ofconnexin 43 in humantesticular seminomacells: overexpressionof Cx43 inducesmembrane location andcell proliferationdecrease C. RogerBaharia MograbiD. Chevallier2004 год

Disrupted traffic of connexin 43 in human testicular seminoma cells: overexpression of Cx43 induces membrane location and cell proliferation decrease
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Аннотация: Abstract Connexins, the constitutive proteins of gap junctions, are considered to be tumour suppressive agents and are often impaired in the tumourigenic processes. In the present study, the expression of connexin 43 (Cx43), which is involved in the control of spermatogenesis through Sertoli/germ cell coupling, has been investigated in human testicular seminoma cells (tumours and the JKT‐1 cell line). Cx43 was immunolocalized in the Golgi apparatus without membrane expression and was detected by immunoblotting in JKT‐1 as exclusive 70 kD bands. No mutation could be found by sequencing the transcript obtained by RT‐PCR. Transfection with a Cx43‐V5 vector reproduced the same gel shift, identifying these 70 kD bands as Cx43. The Cx43‐70 kD bands were also expressed in normal testicular tissue, associated with the classical 43 kD isoforms. Stable transfection of JKT‐1 with a Cx43‐GFP vector allowed restoration of Cx43 membrane expression, functional cell coupling, and inhibition of the cell proliferation rate. Storage of Cx43 in the Golgi apparatus may correspond during spermatogenesis to an intermittent physiological process that becomes permanent in malignant seminoma cells as a result of the tumourigenic process. By preventing Cx43 membrane expression, this disrupted traffic may itself participate in tumour promotion. Copyright © 2004 John Wiley & Sons, Ltd.
Год издания: 2004
Авторы: C. Roger, Baharia Mograbi, D. Chevallier, J Michiels, Hiroyoshi Tanaka, Dominique Segretain, Georges Pointis, Patrick Fénichel
Источник: The Journal of Pathology
Ключевые слова: Connexins and lens biology, Heat shock proteins research, Prostate Cancer Diagnosis and Treatment
Другие ссылки: The Journal of Pathology (HTML)
PubMed (HTML)