Abstract
Chronic inflammation is a major cause of human cancers. The environmental factors, such as microbiome, dietary components, and obesity, provoke chronic inflammation in the prostate, which promotes cancer development and progression. Crosstalk between immune cells and cancer cells enhances the secretion of intercellular signaling molecules, such as cytokines and chemokines, thereby orchestrating the generation of inflammatory microenvironment. Tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs) play pivotal roles in inflammation-associated cancer by inhibiting effective anti-tumor immunity. Anti-inflammatory agents, such as aspirin, metformin, and statins, have potential application in chemoprevention of prostate cancer. Furthermore, pro-inflammatory immunity-targeted therapies may provide novel strategies to treat patients with cancer. Thus, anti-inflammatory agents are expected to suppress the “vicious cycle” created by immune and cancer cells and inhibit cancer progression. This review has explored the immune cells that facilitate prostate cancer development and progression, with particular focus on the application of anti-inflammatory agents for both chemoprevention and therapeutic approach in prostate cancer.
Highlights
Chronic inflammation plays a major role in the etiology and development of various types of malignant tumors, including hepatocellular carcinoma, gastric cancer, lung cancer, colorectal cancer, and prostate cancer [1,2,3,4,5]
Inherited germline mutations are involved in prostate cancer development [6,7], immigration studies indicate the importance of environmental factors; for instance, it was found that immigrants from Asian countries in Western countries acquired higher prostate cancer risks within one generation [8,9]
Chronic inflammation plays a major role in the etiology, development, and progression of prostate cancer
Summary
Chronic inflammation plays a major role in the etiology and development of various types of malignant tumors, including hepatocellular carcinoma, gastric cancer, lung cancer, colorectal cancer, and prostate cancer [1,2,3,4,5]. The first prospective study in men without biopsy indication revealed that benign tissue inflammation was positively associated with prostate cancer development [32]. The progression and aggressiveness of prostate cancer was reportedly associated with systemic inflammation markers in the serum, such as C-reactive protein levels, as well as differential blood cell count (neutrophils, lymphocytes, monocytes, and platelets) [33,34,35,36,37]. Accumulated DNA damage can cause somatic mutations in key tumor suppressor genes and induce genome instability resulting in genomic changes in oncogenes, facilitating the development and progress of prostate cancer [3,42,43]. Anti-inflammatory agents are expected to suppress inflammation in the tumor microenvironment and inhibit prostate cancer progression (Figure 1). We have reviewed the immune cells that facilitate prostate cancer development and progression, and especially focused on the application of anti-inflammatory agents for both chemoprevention and therapeutic approach in prostate cancer
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
