Comparison of contact-mediated communication in normal and transformed human cells in culture.

Corsaro, Cheryl M.; Migeon, Barbara R.

doi:10.1073/pnas.74.10.4476

Cited by 48 publications

(12 citation statements)

References 31 publications

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“…Spontaneously occurring cell lines derived from tumors have been found to be either defective or nonselective in junctional communication (13,39 …”

Section: Discussionmentioning

confidence: 99%

“…The transfection experiments followed the procedure described by Wigler et al (24). The total DNA per plate was 20 ,ug which includes plasmid DNA (0-10 ,ug per plate) and salmon DNA (10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) ,tg per plate). After 5 hr of incubation with calcium phosphate/DNA precipitate, the medium was removed and the attached cells were treated with 20% glycerol in phosphate-buffered saline (P1/NaCl) for 1 min.…”

Section: Methodsmentioning

confidence: 99%

“…Of the many phenotypic changes that are associated with malignant transformation, the loss of contact inhibition and gap-junctional communication has been postulated to play a significant role (12)(13)(14). The demonstration that phorbol 12-myristate 13-acetate (PMA) (15,16), teleocidin (17), and other promoters (18) can inhibit gap-junctional intercellular communication, reversibly, suggests a possible mechanism by which growth-promoting oncogenes might influence transformation.…”

mentioning

confidence: 99%

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Potential role of the src gene product in inhibition of gap-junctional communication in NIH/3T3 cells.

Chang

Trosko

Kung

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

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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-l1). Six transformed clones that were studied contained newly incorporated v-src genes in the genome, had an increased amount of pp6src, 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.The identification of the role of many genes involved in the complex multistep carcinogenic process has begun with the development of techniques to detect oncogenes in vitro (1). The recent demonstrations that some oncogenes code for a growth factor (2-4), growth factor receptor (5), and several tyrosine-directed protein kinases (6) suggest that many of these oncogenes have growth-promoting effects. More recently, the discovery that some oncogene products can phosphorylate phosphatidylinositol (7,8) MATERIALS AND METHODSIsolation of src Gene-Transformed NIH/3T3 Clones. NIH/3T3 cells, used as DNA recipients, were grown in Dulbecco's modified minimal essential medium supplemented with 10% fetal calf serum at 37°C in water-jacketed incubators that provide 5% CO2 in air and humidity. The donor DNA carrying the v-src gene is a plasmid (psrc"l) provided to us by G. Cooper (Harvard Medical School). This plasmid contains an intact Rous sarcoma virus v-src gene with two long terminal repeat promoters positioned both upstream and downstream from the gene, in such a way that the v-src messages can be effectively expressed (see Fig. 10. The transfection experiments followed the procedure described by Wigler et al. (24). The total DNA per plate was 20 ,ug which includes plasmid DNA (0-10 ,ug per plate) and salmon DNA (10-20 ,tg per plate). After 5 hr of incubation with calcium phosphate/DNA precipitate, the medium was removed and the attached cells were treated with 20% glycerol in phosphate-buffered saline (P1/NaCl) for 1 min.After rinsing with Pi/NaCl, fresh medium was added to each plate. The cells were cultured for 2 weeks with a change of medium every 3 days before the plates were overlayed with 0.28% agarose. After an additional week, colonies that developed into the soft agar were isolated for further studies.Iletermination of the Presence of Transfected src Gene in NIH/3T3 Clones. DNA of NIH/3T3 clones was isolated by the procedure of Maniatis et al. (25). Forty micrograms of DNA from each cell line was dig...

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“…Spontaneously occurring cell lines derived from tumors have been found to be either defective or nonselective in junctional communication (13,39 …”

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Potential role of the src gene product in inhibition of gap-junctional communication in NIH/3T3 cells.

Chang

Trosko

Kung

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

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“…In liver, various functions are regulated by cell-cell contact, and expression of hepatocyte-specific characters may not be stabilized unless the cells form tissue and receive complex regulation from their cytosocial environment. In contrast, transformed cells do not respond to their environment, and transformation or dedifferentiation is usually accompanied by loss of contact inhibition of growth (11)(12)(13)(14). This defective contact-inhibition of mobility of malignant cells also contributes to their invasiveness (15).…”

mentioning

confidence: 99%

Loss of reciprocal modulations of growth and liver function of hepatoma cells in culture by contact with cells or cell membranes.

Nakamura¹,

Nakayama²,

Teramoto³

et al. 1984

Proc. Natl. Acad. Sci. U.S.A.

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In mature rat hepatocytes in primary culture, many metabolic functions and cell growth are controlled reciprocally by cell density, and this reciprocal regulation is mediated by a cell-surface modulator through cell-cell contact. Cultured RY-121B cells from Reuber hepatoma and MH1Cj cells from Morris hepatoma, which retain some liverspecific functions, did not show any cell-density dependency of either cell growth or hepatocyte-specific functions, such as induction of tyrosine aminotransferase by dexamethasone. However, when RY-121B cells were cocultured with a low density of rat hepatocytes as monolayers in direct contact, they exerted contact-dependent control of DNA synthesis and of differentiated function of the hepatocytes. Furthermore, plasma membranes from various tumor cells including these hepatoma cells had strong modulator activity on primary cultures of normal rat hepatocytes, and their activity mimicked the reciprocal effects of cell density on DNA synthesis and induction of tyrosine aminotransferase. On the contrary, addition of plasma membranes from normal adult rat liver to sparse cultures of RY-121B or MH1Cj cells did not cause any inhibition of active DNA synthesis or enhancement of induction of tyrosine aminotransferase in these cells. These results suggest that hepatoma cells have lost cell density-dependent regulations of many cellular activities and cell growth because they have lost the ability to respond to the cell surface modulator, although they retain modulator activity on their plasma membranes.

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“…The alteration in phosphorylation of gap junction molecules following TPA treatment for 1 hr has been demonstrated (Hertzberg, personal communication, 19911, suggesting a direct effect of TPA on gap junction proteins. Furthermore, a correlation has been demonstrated between junctional communication, alteration of rate of cell proliferation, and cell transformation (Trosko et al, 1982;Loewenstein, 1974;Sheridan and Johnson, 1975;Corsaro and Migeon, 1979).…”

Section: T -mentioning

confidence: 95%

Regulation of the 12‐o‐tetradecanoyl‐phorbol‐13‐acetate‐induced inhibition of intercellular communication

et al. 1993

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Effects of the tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and protein kinase C (PKC) inhibitors on cell-cell communication were studied in a normal rat liver cell line, clone 9. Communication was observed and quantitated with microspectofluorometric and image analysis techniques following scrape-loading of the cells with lucifer yellow. Lucifer yellow migrated as far as ten cells away from the scraped edge in control populations. Two minute TPA (25-50 micrograms/ml) treatment inhibited dye movement such that the dye remained mainly in the cells at the cut edge. The TPA-induced inhibition of cell-cell communication could be partially blocked by 15 min treatment of the cell populations with the PKC inhibitors trifluoperazine (30 micrograms/ml), staurosporine (2 x 10(-8) or 2 x 10(-6) M), sangivamycin (15 or 200 microM), or a PKC inhibitor peptide (20 micrograms/ml) scraped in at the same time as lucifer yellow. Normal communication was observed in cultures treated only with PKC inhibitors. Lower concentrations of TPA (50 ng/ml-1 micrograms/ml) used for 2 min did not inhibit dye communication. Our results demonstrate the phorbol ester-induced interruption of cell-cell communication. The inhibition of PKC by inhibitors eliminates the effect of TPA on communication. Our data are consistent with a role of PKC in the control of junctional communication.

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Comparison of contact-mediated communication in normal and transformed human cells in culture.

Abstract: With an assay that quantitates the transfer of 6-thioguanylic acid from hypoxanthine phosphoribosyltransferase (IMP:pyrophosphate

Cited by 48 publications

References 31 publications

Potential role of the src gene product in inhibition of gap-junctional communication in NIH/3T3 cells.

Potential role of the src gene product in inhibition of gap-junctional communication in NIH/3T3 cells.

Loss of reciprocal modulations of growth and liver function of hepatoma cells in culture by contact with cells or cell membranes.

Regulation of the 12‐o‐tetradecanoyl‐phorbol‐13‐acetate‐induced inhibition of intercellular communication

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