Enhancement of natural-killer-cell susceptibility of human breast-cancer cells by estradiol and v-Ha-ras oncogene

I. Screpanti, M. P. Felli, E. Toniato, D. Meco, S. Martinotti, L. Frati, A. Santoni, A. Gulino

Research output: Contribution to journalArticle

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Abstract

Natural killer (NK) cells are putative components of the cellular immune response to transformed cells. Since both estradiol treatment and ras-oncogene overexpression enhance tumorigenicity of hormone-dependent breast-cancer cells, we studied the effects of estrogen and of the activated v-Ha-ras oncogene on NK susceptibility of MCF-7 human breast-cancer cells. MCF-7 cells were sensitive to cytolysis mediated by resting and IL2-activated peripheral-blood non-adherent lymphocytes. Lysis appeared to be mediated by NK cells, since it was abrogated by treatment of effector cells with α-CD16 monoclonal antibody (MAb) plus complement (c'). Estradiol treatment of MCF-7 cells was able to significantly increase their sensitivity to the lysis by IL2-activated and unactivated peripheral-blood lymphocytes, as early as 24 hr throughout 10 days of hormone treatment. Hormone-insensitive, estrogen-receptor-negative breast-cancer cells (BT20) did not change their NK susceptibility after estradiol treatment. Increased NK susceptibility was also observed in v-Ha-ras-transfected and oncogene product overexpressing MCF-7 cells (MCF-7-ras) with respect to cells transfected with the selectable gene marker gpt alone (MCF-7-gpt). Overexpression of v-Ha-ras appeared to be able to bypass the need for estrogen to increase NK susceptibility, since estradiol-treated MCF-7 ras cells were not lysed more than untreated MCF-7-ras cells. The enhancement of NK susceptibility observed after both estradiol treatment and v-Ha-ras overexpression suggests that the hormone-mediated and the ras-oncogene-mediated signalling systems share events involved in the control of tumor-cell/host-effector-cell interactions.

Original languageEnglish
Pages (from-to)445-449
Number of pages5
JournalInternational Journal of Cancer
Volume47
Issue number3
Publication statusPublished - 1991

Fingerprint

ras Genes
Natural Killer Cells
Estradiol
MCF-7 Cells
Breast Neoplasms
Hormones
Interleukin-2
Estrogens
Lymphocytes
Oncogene Proteins
Population Growth
Cellular Structures
Cellular Immunity
Cell Communication
Estrogen Receptors
Monoclonal Antibodies
Genes
Neoplasms

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Screpanti, I., Felli, M. P., Toniato, E., Meco, D., Martinotti, S., Frati, L., ... Gulino, A. (1991). Enhancement of natural-killer-cell susceptibility of human breast-cancer cells by estradiol and v-Ha-ras oncogene. International Journal of Cancer, 47(3), 445-449.

Enhancement of natural-killer-cell susceptibility of human breast-cancer cells by estradiol and v-Ha-ras oncogene. / Screpanti, I.; Felli, M. P.; Toniato, E.; Meco, D.; Martinotti, S.; Frati, L.; Santoni, A.; Gulino, A.

In: International Journal of Cancer, Vol. 47, No. 3, 1991, p. 445-449.

Research output: Contribution to journalArticle

Screpanti, I, Felli, MP, Toniato, E, Meco, D, Martinotti, S, Frati, L, Santoni, A & Gulino, A 1991, 'Enhancement of natural-killer-cell susceptibility of human breast-cancer cells by estradiol and v-Ha-ras oncogene', International Journal of Cancer, vol. 47, no. 3, pp. 445-449.
Screpanti, I. ; Felli, M. P. ; Toniato, E. ; Meco, D. ; Martinotti, S. ; Frati, L. ; Santoni, A. ; Gulino, A. / Enhancement of natural-killer-cell susceptibility of human breast-cancer cells by estradiol and v-Ha-ras oncogene. In: International Journal of Cancer. 1991 ; Vol. 47, No. 3. pp. 445-449.
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