دورية أكاديمية
alpha-Catulin Drives Metastasis by Activating ILK and Driving an alpha v beta 3 Integrin Signaling Axis
العنوان: | alpha-Catulin Drives Metastasis by Activating ILK and Driving an alpha v beta 3 Integrin Signaling Axis |
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المؤلفون: | Liang, Chen-Hsien, Chiu, Szu-Ying, Hsu, I-Ling, Wu, Yi-Ying, Tsai, Yao-Tsung, Ke, Jhen-Yu, Pan, Szu-Hua, Hsu, Yi-Chiung, Li, Ker-Chau, Yang, Pan-Chyr, Chen, Yuh-Ling, Hong, Tse-Ming |
المساهمون: | Graduate Institute of Clinical Medicine |
بيانات النشر: | American Association for Cancer Research |
سنة النشر: | 2013 |
المجموعة: | National Cheng Kung University: NCKU Institutional Repository / 國立成功大學機構典藏 |
الوصف: | alpha-Catulin is an oncoprotein that helps sustain proliferation by preventing cellular senescence. Here, we report that alpha-catulin also drives malignant invasion and metastasis. alpha-Catulin was upregulated in highly invasive non-small cell lung cancer (NSCLC) cell lines, where its ectopic expression or short-hairpin RNA-mediated attenuation enhanced or limited invasion or metastasis, respectively. alpha-Catulin interacted with integrin-linked kinase (ILK), a serine/threonine protein kinase implicated in cancer cell proliferation, antiapoptosis, invasion, and angiogenesis. Attenuation of ILK or alpha-catulin reciprocally blocked cell migration and invasion induced by the other protein. Mechanistic investigations revealed that alpha-catulin activated Akt-NF-kappa B signaling downstream of ILK, which in turn led to increased expression of fibronectin and integrin alpha v beta 3. Pharmacologic or antibody-mediated blockade of NF-kappa B or alpha v beta 3 was sufficient to inhibit alpha-catulin-induced cell migration and invasion. Clinically, high levels of expression of alpha-catulin and ILK were associated with poor overall survival in patients with NSCLC. Taken together, our study shows that alpha-catulin plays a critical role in cancer metastasis by activating the ILK-mediated Akt-NF-kappa B-alpha v beta 3 signaling axis. Cancer Res; 73(1); 428-38. (C)2012 AACR. |
نوع الوثيقة: | article in journal/newspaper |
اللغة: | English |
العلاقة: | Cancer Research, Vol. 73, No. 1, pp. 428-438; http://ir.lib.ncku.edu.tw/handle/987654321/143306Test; http://ir.lib.ncku.edu.tw/bitstream/987654321/143306/-1/index.htmlTest |
DOI: | 10.1158/0008-5472.CAN-12-2095 |
الإتاحة: | https://doi.org/10.1158/0008-5472.CAN-12-2095Test http://ir.lib.ncku.edu.tw/handle/987654321/143306Test http://ir.lib.ncku.edu.tw/bitstream/987654321/143306/-1/index.htmlTest |
رقم الانضمام: | edsbas.18013665 |
قاعدة البيانات: | BASE |
DOI: | 10.1158/0008-5472.CAN-12-2095 |
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