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Lectin-resistant B16 melanoma cells exhibit an altered response to MSH and cholera toxin
Abstract:
Mouse B16 melanoma cells respond to melanocyte-stimulating hormone (MSH) or cholera toxin (CT) with an accumulation of cAMP. The kinetics and dose-response of MSH were examined in the B16 parent line and two cell clones derived from it that exhibited wheat germ agglutinin (WGA) resistance [1]. These WGA lectin-resistant cells, designated W4 and W5 showed a greater response to MSH and CT than the parent B16 cells. Exposure of the W4 and W5 cells to lotus lectin or ricin respectively, led to the previously described [2] selection of cell clones that were resistant to lotus lectin (W4L) and ricin (W5R). The W4L and W5R cells which were shown [2] to be as sensitive as the B16 parent to WGA (i.e., were phenotypically reverted to WGA sensitivity), were also found to respond to MSH in a manner similar to the B16 parent. Since lectin sensitivity has been directly correlated in these cell clones with the membrane's oligosaccharides and glycopeptide pattern, these data suggest that the cellular binding and/or biological response to hormones is influenced by the carbohydrate composition of the plasma membrane.
Insights
Mouse melanoma cells show altered responses to hormones based on their cell surface carbohydrate patterns. Changes in cell surface sugars, identified through lectin resistance, impact hormone signaling pathways.
Area of Science:
- Cell Biology
- Biochemistry
- Molecular Endocrinology
Background:
- Mouse B16 melanoma cells exhibit cAMP accumulation in response to melanocyte-stimulating hormone (MSH) and cholera toxin (CT).
- Lectin resistance in cell lines is often associated with alterations in cell surface oligosaccharides and glycopeptide patterns.
Purpose of the Study:
- To investigate the relationship between cell surface carbohydrate composition and cellular responses to hormones.
- To examine the impact of lectin resistance on MSH-induced cAMP accumulation in B16 melanoma cells.
Main Methods:
- Utilized B16 melanoma parent cell line and derived wheat germ agglutinin (WGA)-resistant clones (W4, W5).
- Assessed MSH and CT dose-response and kinetics.
- Selected lotus lectin-resistant (W4L) and ricin-resistant (W5R) clones from W4 and W5 cells.
- Correlated lectin sensitivity with cell surface glycopeptide patterns.
Main Results:
- WGA-resistant cells (W4, W5) displayed enhanced responses to MSH and CT compared to parent B16 cells.
- Lotus lectin-resistant (W4L) and ricin-resistant (W5R) cells, phenotypically reverted to WGA sensitivity, showed MSH responses similar to the parent B16 cells.
- Lectin sensitivity was directly correlated with the plasma membrane's oligosaccharide and glycopeptide composition.
Conclusions:
- Cellular binding and biological responses to hormones are influenced by the carbohydrate composition of the plasma membrane.
- Alterations in cell surface glycosylation can modulate hormone signaling pathways in melanoma cells.