Altered levels of endogenous retrovirus‐like sequence (VL30) RNA during mouse epidermal cell carcinogenesis

Gene expression during mouse keratinocyte carcinogenesis was examined in a clonal cell model. Tumor cells from three separate initiated cell lineages were compared with their nontumorigenic precursors and with the progenitor cell strain prior to treatment with 7,12‐dimethylbenzaanthracene (DMBA). The steady‐state levels of VL30 RNA in normal and papilloma cells were regulated by extracellular Ca²⁺ (which controls proliferation and differentiation in normal epidermal keratinocytes) and culture density. In contrast, steady‐state levels of VL30 RNA were not regulated by these factors in the squamous cell carcinoma or the anaplastic carcinoma cells. VL30 expression was Ca²⁺ dependent in the initiated cell precursors within each tumor cell lineage, suggesting that the loss of response to extracellular Ca²⁺ was associated with the malignant conversion stage of carcinogenesis. No differences between normal and tumor cells were found in the cellular RNA levels of five additional proto‐oncogenes. The mouse epidermal cell model should provide a means for direct assessment of a potential functional role of VL30 sequences in cancer development.