Prostate cancer metastasis: Role of the host microenvironment in promoting epithelial to mesenchymal transition and increased bone and adrenal gland metastasis

The Prostate ◽  
2006 ◽  
Vol 66 (15) ◽  
pp. 1664-1673 ◽  
Author(s):  
Jianchun Xu ◽  
Ruoxiang Wang ◽  
Zhi Hui Xie ◽  
Valerie Odero-Marah ◽  
Sen Pathak ◽  
...  
2021 ◽  
Vol 22 (10) ◽  
pp. 5078
Author(s):  
Andy Göbel ◽  
Stefania Dell'Endice ◽  
Nikolai Jaschke ◽  
Sophie Pählig ◽  
Amna Shahid ◽  
...  

Tumor metastasis to bone is a common event in multiple forms of malignancy. Inflammation holds essential functions in homeostasis as a defense mechanism against infections and is a strategy to repair injured tissue and to adapt to stress conditions. However, exaggerated and/or persistent (chronic) inflammation may eventually become maladaptive and evoke diseases such as autoimmunity, diabetes, inflammatory tissue damage, fibrosis, and cancer. In fact, inflammation is now considered a hallmark of malignancy with prognostic relevance. Emerging studies have revealed a central involvement of inflammation in several steps of the metastatic cascade of bone-homing tumor cells through supporting their survival, migration, invasion, and growth. The mechanisms by which inflammation favors these steps involve activation of epithelial-to-mesenchymal transition (EMT), chemokine-mediated homing of tumor cells, local activation of osteoclastogenesis, and a positive feedback amplification of the protumorigenic inflammation loop between tumor and resident cells. In this review, we summarize established and evolving concepts of inflammation-driven tumorigenesis, with a special focus on bone metastasis.


2018 ◽  
Vol Volume 10 ◽  
pp. 4029-4038 ◽  
Author(s):  
Fei Zhan ◽  
Jingling Shen ◽  
Ruitao Wang ◽  
Liang Wang ◽  
Yao Dai ◽  
...  

2008 ◽  
Vol 7 (11) ◽  
pp. 1849-1851 ◽  
Author(s):  
Candece L. Gladson ◽  
Danny R. Welch

2020 ◽  
Vol Volume 13 ◽  
pp. 7411-7422 ◽  
Author(s):  
Lin Tang ◽  
Meng Xu ◽  
Long Zhang ◽  
Lin Qu ◽  
Xiaoyan Liu

2020 ◽  
pp. 1-23
Author(s):  
Divya Adiga ◽  
Raghu Radhakrishnan ◽  
Sanjiban Chakrabarty ◽  
Prashant Kumar ◽  
Shama Prasada Kabekkodu

Despite substantial advances in the field of cancer therapeutics, metastasis is a significant challenge for a favorable clinical outcome. Epithelial to mesenchymal transition (EMT) is a process of acquiring increased motility, invasiveness, and therapeutic resistance by cancer cells for their sustained growth and survival. A plethora of intrinsic mechanisms and extrinsic microenvironmental factors drive the process of cancer metastasis. Calcium (Ca<sup>2+</sup>) signaling plays a critical role in dictating the adaptive metastatic cell behavior comprising of cell migration, invasion, angiogenesis, and intravasation. By modulating EMT, Ca<sup>2+</sup> signaling can regulate the complexity and dynamics of events leading to metastasis. This review summarizes the role of Ca<sup>2+</sup> signal remodeling in the regulation of EMT and metastasis in cancer.


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