PulseExploreJournal ClubDebatesTrendingResearchersJournals
Instagram
HomeExploreJournal ClubTrending
Synapse
⌘+K
Synapse
November 1, 1989The Journal of Experimental Medicine152 citationsOpen Access

Interleukin 6 decreases cell-cell association and increases motility of ductal breast carcinoma cells.

ITIgor TammICIrma CardinaleJKJames G. Krueger

Key Points

Key points are not available for this paper at this time.

Abstract

Treatment of transformed breast duct epithelial cells with IL-6 produces a unique cellular phenotype characterized by diminished proliferation and increased motility. Human ductal carcinoma cells (T-47D and ZR-75-1 lines) are typically epithelioid in shape and form compact colonies in culture. Time-lapse cinemicrography shows that some untreated cells can transiently become fusiform or stellate in shape and separate from each other within a colony, but they usually rejoin their neighbors. While IL-6 suppresses the proliferation of these carcinoma cells, the IL-6-treated cells generally become stellate or fusiform and show increased motility. These changes persist as long as the cells are exposed to IL-6. This results in the dispersal of cells within colonies. The effects on cell growth, shape, and motility are reversible upon removal of IL-6. IL-6-treated T-47D cells display diminished adherens-type cell junctions, as indicated by markedly decreased vinculin-containing adhesions and intercellular desmosomal attachments. The effects on ZR-75-1 cell shape, colony number, and DNA synthesis are dependent on IL-6 concentration in the range from 0.15 to 15 ng/ml. Higher concentrations are required in T-47D cells for equivalent effects. Anti-IL-6 immune serum blocks IL-6 action. IL-6 represents a well-characterized molecule that regulates both the proliferation and junction-forming ability of breast ductal carcinoma cells.

Ask AI
Helpful
Bookmark
Share
View Full Paper

Cite This Study

Tamm et al. (1989) studied this question.

synapsesocial.com/papers/6a637e5f93e7e2232d286d0ahttps://doi.org/10.1084/jem.170.5.1649
Ask AI
Helpful
Bookmark
Share
View Full Paper