Molecular mechanism of cancer cell pluripotency responding to stress

癌细胞多能性响应应激的分子机制

• 批准号: 24659149
• 负责人: KANEDA Yasufumi
• 金额: $ 2.5万
• 依托单位: Osaka University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Challenging Exploratory Research
• 财政年份: 2012
• 资助国家: 日本
• 起止时间: 2012-04-01 至 2014-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-24659149/
• 关键词: 癌幹細胞; 抗がん剤耐性; 前立腺がん; 多能性維持因子; ストレス応答; 抗癌剤耐性; 前立腺癌

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.

尽管多西他赛难治性前列腺癌患者的患病率越来越高，但对其肿瘤生物学的了解知之甚少。在这项研究中，我们证明，与亲本的前列腺癌细胞相比，多西他赛的残留前列腺癌细胞中的肿瘤潜能增加。 CXCR4，ERK1/2和C-MYC信号回路激活控制了增强的肿瘤电位。此外，在抗多西他赛耐药前列腺癌患者的临床癌组织样品中证明了组成型CXCR4，ERK1/2和C-MYC信号传导激活。这些信号通路可能成为化学疗法后抑制侵袭性残留肿瘤细胞的治疗靶标。

项目成果

大阪大学大学院医学系研究科遺伝子治療学ホームページ

大阪大学医学研究科基因治疗主页

大阪大学大学院学系研究科遺伝子治療学

大阪大学基因治疗研究科

Future direction of gene therapy

基因治疗的未来方向

• 发表时间: 2012
• 作者: Hatano K;Yamaguchi S;Nimura K;Murakami K;Nagahara A;Fujita K;Uemura M;Nakai Y;Tsuchiya M;Nakayama M;Nonomura N;*Kaneda Y.;金田安史;金田安史
• 通讯作者: 金田安史

Future directions of gene therapy

基因治疗的未来方向

• 发表时间: 2012
• 作者: Hatano K;Yamaguchi S;Nimura K;Murakami K;Nagahara A;Fujita K;Uemura M;Nakai Y;Tsuchiya M;Nakayama M;Nonomura N;*Kaneda Y.;金田安史;金田安史;金田安史
• 通讯作者: 金田安史

Residual Prostate Cancer Cells after Docetaxel Therapy Increase the Tumorigenic Potential via Constitutive Signaling of CXCR4, ERK1/2 and c-Myc

• DOI: 10.1158/1541-7786.mcr-13-0029-t
• 发表时间: 2013-09-01
• 期刊: MOLECULAR CANCER RESEARCH
• 影响因子: 5.2
• 作者: Hatano, Koji;Yamaguchi, Souhei;Kaneda, Yasufumi
• 通讯作者: Kaneda, Yasufumi