Reynolds N J, Todd C, Angus B
Department of Dermatology, University of Newcastle, Newcastle upon Tyne, UK.
Br J Dermatol. 1997 May;136(5):666-73.
Protein kinase C (PKC) isoenzymes transduce signals from cell surface receptors and thereby regulate important cellular functions in skin including keratinocyte growth and differentiation. Overexpression of individual PKC isoenzymes results in aberrant cell growth and in certain instances tumorigenicity. PKC is implicated in tumour promotion in mouse skin. Abnormal expression of PKC has been reported in several human cancers. We have, therefore, investigated expression of PKC-alpha and -beta in basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) by immunohistochemistry. Sections were stained with specific antibodies to PKC-alpha, PKC-beta, CD1a, T cells, B cells and dermal dendritic cells (factor XIIIa), using an immunoperoxidase technique. PKC-alpha and PKC-beta were not detected in tumour cells in BCCs or SCCs. In SCCs, PKC-beta immunostaining revealed positively stained inflammatory and dendritic cells scattered through the stroma; PKC-alpha immunostaining was essentially negative. In contrast, in BCCs, PKC-alpha+ and PKC-beta+ dendritic and spindle-shaped cells were observed in the stroma, immediately adjacent to the tumour islands. Double-labelling experiments showed that a proportion (approximately 20%) of PKC-beta+ dendritic cells also expressed factor XIIIa. BCCs depend on stroma for growth; PKC regulates expression of type IV collagenase and stromelysin III and interactions between tumour and stroma may be important in determining tumour invasion and metastasis. Therefore, overexpression of PKC-alpha and -beta by stromal dendritic cells in BCCs suggests that PKC activation may be involved in stromal/tumour interactions in these tumours.
蛋白激酶C（PKC）同工酶可转导来自细胞表面受体的信号，从而调节皮肤中重要的细胞功能，包括角质形成细胞的生长和分化。单个PKC同工酶的过表达会导致细胞生长异常，并在某些情况下导致肿瘤发生。PKC与小鼠皮肤的肿瘤促进有关。已有报道称PKC在几种人类癌症中表达异常。因此，我们通过免疫组织化学研究了基底细胞癌（BCC）和鳞状细胞癌（SCC）中PKC-α和-β的表达。使用免疫过氧化物酶技术，用针对PKC-α、PKC-β、CD1a、T细胞、B细胞和真皮树突状细胞（因子XIIIa）的特异性抗体对切片进行染色。在BCC或SCC的肿瘤细胞中未检测到PKC-α和PKC-β。在SCC中，PKC-β免疫染色显示散在分布于基质中的炎性细胞和树突状细胞呈阳性染色；PKC-α免疫染色基本为阴性。相反，在BCC中，在紧邻肿瘤岛的基质中观察到PKC-α+和PKC-β+的树突状细胞和梭形细胞。双重标记实验表明，一部分（约20%）PKC-β+树突状细胞也表达因子XIIIa。BCC的生长依赖于基质；PKC调节IV型胶原酶和基质溶解素III的表达，肿瘤与基质之间的相互作用可能对确定肿瘤的侵袭和转移很重要。因此，BCC中基质树突状细胞PKC-α和-β的过表达表明PKC激活可能参与了这些肿瘤的基质/肿瘤相互作用。
