Regulation of murine plasmacytoma transferrin receptor expression and G1 traversal by plasmacytoma cell growthfactor

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Abstract
Many plasmacytomas arising in BALB/c mice require a specific, macrophage-derived growth factor in order to proliferate in vitro. Since transferin receptor expression is normally regulated by tissue-specific growth factors and because expression of these receptors is required for cell proliferation, we examined the interaction of plasmacytoma growth factor (PCT-GF) on transferrin receptor expression and cell cycle progression in several PCT-GF-dependent and independent plasmacytoma cell lines maintained in vitro. We found that removal of PCT-GF results in a rapid and specific loss of transferrin receptor expression with concomitant G1 arrest in early G1. The time required for G1 arrest to become maximal correlates closely to the initial level of surface transferrin receptor expression and the rate of decay following removal of PCT-GF. The calcium channel blocker diltiazem interferes with the ability of PCT-GF to maintain transferrin receptor expression in PCT-GF-dependent cell lines and causes a G1 arrest of the cell population. When added to a PCT-GF-independent cell line, diltiazem also inhibited transferrin receptor expression and caused G1 arrest. Thus, both PCT-GF-dependent and -independent plasmacytoma cell lines require transferrin receptor expression for growth. In factor dependent cell lines, transferrin receptor expression requires exogenous PCT-GF, while in factor-independent cells, transferrin receptor expression is constitutive. In both cell types, intracellular calcium levels may play a role in receptor expression.