Goel R, Kaul D, Varma S
Department of Experimental Medicine & Biotechnology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Leuk Res. 1996 Oct;20(10):877-9. doi: 10.1016/s0145-2126(96)00030-6.
Deranged cellular cholesterol homeostasis has been widely recognized in the initiation as well as progression of various types of cancers including chronic myeloid leukaemia (CML). Since the human genomic sterol regulatory element (SRE) has been shown to regulate various key genes involved in this phenomenon, the present study revealed the existence of a unique 47 kDa protein factor having affinity for this SRE sequence in lymphocytes from normal subjects, as well as its absence in lymphocytes from untreated CML patients. However, this factor appeared when these CML patients achieved complete haematological remission (CHR) through alpha-interferon therapy. Furthermore, an inverse relationship was also observed between the LDL receptor gene expression at the transcriptional level and the binding affinity of this 47 kDa protein factor to the SRE sequence. Based upon these results we propose that this factor may have a role in pathophysiology of chronic myeloid leukaemia.
细胞胆固醇稳态紊乱在包括慢性粒细胞白血病（CML）在内的各种癌症的发生和发展过程中已得到广泛认可。由于人类基因组固醇调节元件（SRE）已被证明可调节参与这一现象的各种关键基因，本研究揭示，正常受试者淋巴细胞中存在一种对该SRE序列具有亲和力的独特47 kDa蛋白因子，而未经治疗的CML患者的淋巴细胞中则不存在这种因子。然而，当这些CML患者通过α-干扰素治疗实现完全血液学缓解（CHR）时，这种因子会出现。此外，在转录水平上，低密度脂蛋白受体基因表达与这种47 kDa蛋白因子对SRE序列的结合亲和力之间也观察到负相关关系。基于这些结果，我们提出该因子可能在慢性粒细胞白血病的病理生理学中发挥作用。
