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在研究恶性细胞转化的分子基础时,自体分泌生长因子这一概念得到了公认。最近发现癌基因可使癌细胞自主分泌生长因子,从而使癌基因和多肽生长因子两个不同研究领域结合起来。多年来已知:恶性细胞具有相对自主性,也就是说,它们最适生长和增殖所需外源生长因子较相应正常细胞少。为解释这一现象,有人提出:细胞可以产生内源多肽生长因子,作用于它本身外部的活性受体,从而引起细胞对生长因子表型的表达,导致细胞恶变,此过程称为“自体分泌”。这个假说可以解释为什么癌基因能够使癌细胞自体分泌生长因子。如果将正常有丝分裂途径中起关键性控制作用的受体和受体后的信号转导包括在内的话,则此假说更趋完善。这里,概括了一些支持原来的自主分泌假说的实验证据并将此假说加以补充修改以解释一些重要的新的发现。
The concept of autologous secretion of growth factors is well recognized when studying the molecular basis of malignant cell transformation. Recent discovery of oncogenes allows cancer cells to autonomously secrete growth factors, thereby combining two different areas of research on oncogenes and polypeptide growth factors. It has been known for many years that malignant cells are relatively autonomous, that is to say that they require less exogenous growth factors than the corresponding normal cells for optimal growth and proliferation. To explain this phenomenon, it was suggested that cells can produce endogenous peptide growth factor, acting on its own outside of the active receptor, causing cells to express the phenotype of growth factors, resulting in malignant cells, the process is called “autologous secretion ”. This hypothesis explains why oncogenes enable cancer cells to secrete growth factors autonomously. The hypothesis is further refined by including signal transduction of receptors and receptors that play key regulatory roles in normal mitotic pathways. Here, we summarize a few experimental evidence supporting the original autocrine hypothesis and supplement it with this hypothesis to explain some important new findings.