Rosdy M, Bernard B A, Schmidt R, Darmon M
In Vitro Cell Dev Biol. 1986 May;22(5):295-300. doi: 10.1007/BF02621233.
A431 malignant keratinocytes, although derived from a muco-cutaneous carcinoma of the vulva, fail to achieve terminal epidermal differentiation in culture as shown by their inability to form cornified envelopes. Even after culture in a serum-free medium (MCDB 153) containing no retinoic acid and a high (10(-3) M) calcium concentration (conditions known to facilitate epidermal differentiation), the cells do not become competent as shown by the fact that subsequent treatment with a calcium ionophore is unable to provoke the formation of cornified envelopes. Nevertheless, A431 cells are able to synthesize the envelope precursor involucrin. The block in formation of cornified envelopes is thus not due to a lack in involucrin. The results described here suggest that the absence of cross-linking of this molecule is due to a lowered epidermal membrane-bound transglutaminase activity in A431 cells when compared to normal human keratinocytes. In other respects, EGF, which inhibits the proliferation of A431 cells, enhances involucrin accumulation in these cells, although in normal human keratinocytes it stimulates growth and reduces involucrin synthesis. These results suggest that involucrin synthesis is triggered by the arrest of growth.
A431恶性角质形成细胞虽然源自外阴黏膜皮肤癌，但在培养中无法实现终末表皮分化，这表现为它们无法形成角质包膜。即使在不含视黄酸且钙浓度高（10⁻³ M）的无血清培养基（MCDB 153）中培养（已知这种条件有助于表皮分化），细胞也未表现出分化能力，这可从后续用钙离子载体处理无法促使角质包膜形成这一事实得到证明。然而，A431细胞能够合成包膜前体兜甲蛋白。因此，角质包膜形成受阻并非由于兜甲蛋白缺乏。此处所述结果表明，与正常人角质形成细胞相比，A431细胞中该分子交联缺失是由于表皮膜结合转谷氨酰胺酶活性降低。在其他方面，抑制A431细胞增殖的表皮生长因子（EGF）会增强这些细胞中兜甲蛋白的积累，而在正常人角质形成细胞中它会刺激生长并减少兜甲蛋白合成。这些结果表明，兜甲蛋白的合成是由生长停滞触发的。
