Molecular mechanism of cancer cell pluripotency responding to stress

尽管多西他赛难治性前列腺癌患者的患病率越来越高，但对其肿瘤生物学知之甚少。在这项研究中，我们证明了与亲代前列腺癌细胞相比，耐紫杉醇的残留前列腺癌细胞的致瘤潜力增加。CXCR 4、ERK 1/2和c-Myc信号环激活控制了增强的致瘤潜力。此外，组成型CXCR 4，ERK 1/2和c-Myc信号传导激活在来自紫杉醇耐药前列腺癌患者的临床癌组织样品中得到证实。这些信号通路可能成为化疗后抑制侵袭性残留肿瘤细胞的治疗靶点。

Despite an increasing prevalence of patients with docetaxel refractory prostate cancer, little is known about its tumour biology. In this study, we demonstrated that the tumourigenic potential was increased in the docetaxel-resistant residual prostate cancer cells compared with the parental prostate cancer cells. An enhanced tumourigenic potential was controlled by the CXCR4, ERK1/2 and c-Myc signalling loop activation. Furthermore, the constitutive CXCR4, ERK1/2 and c-Myc signalling activation was demonstrated in clinical cancerous tissue samples from human patients with docetaxel-resistant prostate cancer. These signalling pathways may become treatment targets for inhibiting aggressive residual tumour cells after chemotherapy.