Reactive Oxygen Species Bridge the Gap between Chronic Inflammation and Tumor Development

Abstract

According to numerous animal studies, adverse environmental stimuli, including physical, chemical, and biological factors, can cause low-grade chronic inflammation and subsequent tumor development. Human epidemiological evidence has confirmed the close relationship between chronic inflammation and tumorigenesis. However, the mechanisms driving the development of persistent inflammation toward tumorigenesis remain unclear. In this study, we assess the potential role of reactive oxygen species (ROS) and associated mechanisms in modulating inflammation-induced tumorigenesis. Recent reports have emphasized the cross-talk between oxidative stress and inflammation in many pathological processes. Exposure to carcinogenic environmental hazards may lead to oxidative damage, which further stimulates the infiltration of various types of inflammatory cells. In turn, increased cytokine and chemokine release from inflammatory cells promotes ROS production in chronic lesions, even in the absence of hazardous stimuli. Moreover, ROS not only cause DNA damage but also participate in cell proliferation, differentiation, and apoptosis by modulating several transcription factors and signaling pathways. We summarize how changes in the redox state can trigger the development of chronic inflammatory lesions into tumors. Generally, cancer cells require an appropriate inflammatory microenvironment to support their growth, spread, and metastasis, and ROS may provide the necessary catalyst for inflammation-driven cancer. In conclusion, ROS bridge the gap between chronic inflammation and tumor development; therefore, targeting ROS and inflammation represents a new avenue for the prevention and treatment of cancer.

Tumor-associated macrophages in tumor progression and the role of traditional Chinese medicine in regulating TAMs to enhance antitumor effects

“…TAMs could produce IL-1 and TNF-α, promoting the formation of oxygen free radicals and further stimulating the macrophage response to other agonists ( 21 ). Meanwhile, the accumulation of reactive oxygen species (ROS) encourages macrophages to differentiate into a pro-inflammatory state, and therefore participate in the inflammation-induced tumorigenesis ( 22 ).…”

Phytochemical Analysis and Anti-Cancer Properties of Extracts of Centaurea castriferrei Borbás & Waisb Genus of Centaurea L

“…A hallmark of cells in many types of cancers is an imbalance between ROS production and antioxidant defense. Increased levels of ROS, which result from metabolic disturbances at the cellular level and impaired signal transduction, promote carcinogenesis and tumor progression through the activation of oncogenes [ 17 , 18 , 19 ]. On the other hand, further increases in ROS levels in cancer cells can induce irreversible changes and consequent apoptosis—this is how a number of anticancer drugs work, e.g., cisplatin or anthracyclines [ 20 , 21 ].…”

A Novel Systematic Oxidative Stress Score Predicts the Survival of Patients with Early-Stage Lung Adenocarcinoma

“…Therefore, it is necessary to accurately assess the risk of postoperative recurrence in these patients and identify the high-risk group. Previous studies have proposed that ROS is associated with the development of a variety of tumors [ 15 , 22 ], and SOS based on the biomarkers of systematic oxidative stress in peripheral blood, including CRE, TBIL, LDH, BUN, and ALB, have yielded adverse results in the prognostication of breast cancer [ 23 ], but their role in the prognosis of patients with early-stage NSCLC is unclear.…”