Open AccessPotential role of the src gene product in inhibition of gap-junctional communication in NIH/3T3 cells.
Author(s) -
ChiaCheng Chang,
James E. Trosko,
Hsing-Jien Kung,
David W. Bombick,
Fumio Matsumura
Publication year - 1985
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.82.16.5360
Subject(s) - 3t3 cells , transfection , gene product , biology , gene , proto oncogene tyrosine protein kinase src , intracellular , protein kinase c , microbiology and biotechnology , cell culture , kinase , biochemistry , gene expression , genetics
The effects of the src gene on the activity of protein kinase C and intercellular communication have been studied in transformed NIH/3T3 clones isolated from soft agar following transfection with the plasmid carrying the v-src gene (psrc-11). Six transformed clones that were studied contained newly incorporated v-src genes in the genome, had an increased amount of pp60src, and showed enhanced activities of protein kinase C. Intercellular communication, studied by observing with autoradiography the transfer of [3H]uridine nucleotide from prelabeled donor cells to recipient cells in contact, was found to be reduced in transformed clones as compared to parental NIH/3T3 cells. Treatment with phorbol 12-myristate 13-acetate was also found to increase protein kinase C activity and to reduce intercellular communication in normal NIH/3T3 cells. These results suggest that the v-src gene product, in a manner similar to some of the powerful tumor promoters, may directly or indirectly affect cell-cell communication.