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The S100A7/8/9 Proteins: Novel Biomarker and Therapeutic Targets for Solid Tumor Stroma
Published in Surinder K. Batra, Moorthy P. Ponnusamy, Gene Regulation and Therapeutics for Cancer, 2021
Sanjay Mishra, Dinesh Ahirwar, Mohd W. Nasser, Ramesh K. Ganju
S100A8/A9 proteins were also reported to be overexpressed in cutaneous squamous cell carcinoma (SCC) patient samples compared to pre-malignant skin tumors [76]. Ectopic expression of S100A8/A9 in SCC12 cells enhanced proliferation and motility of these cells. When implanted subcutaneously into mice, S100A8/A9 overexpressing SCC12 cells showed enhanced tumor growth [76]. Another study supported SCC promotive role of S100A8/A9 and RAGE. The authors reported that SCC samples have upregulated RAGE and S100A8/A9 compared to normal epidermis and exogenous S100A8/A9 induced SCC keratinocytes in vitro [77]. Exogenous S100A8/A9 activates P38/SAPK/JNK/ERK1/2 signaling pathway to enhance the proliferation of SCC keratinocytes [77]. To identify molecular changes involved in SCC initiation, global genomic DNA methylation was performed and it was observed that S100A8 CpG loci was hypomethylated in SCC tumors compared to adjacent normal tissue [78]. Further analysis showed that S100A8 hypomethylation was associated with reduced overall survival [78]. However, conflicting functions of S100A8/A9 have been reported in SCC. Khammanivong et al. have observed that S100A8/A9 is downregulated in squamous cell carcinomas of the cervix, esophagus, and the head and neck (HNSCC) [79]. Furthermore, ectopic expression of S100A8/A9 suppressed SCC in vitro and in vivo [79]. In addition, another study suggested protective role of S100A9 against SCC using S100A9 knockout mouse model and chemically induced SCC model [80].
Neuroprotection, Aging, and the Gut–Brain Axis
Published in Aruna Bakhru, Nutrition and Integrative Medicine, 2018
The most reliable biomarkers for clinicians to assess gut–brain function are as follows: Microbial diversity—Gut microbiota profiles in a variety of conditions including autism, major depression, and Parkinson's disease show that individuals suffering from ill-health tend to show narrowing in microbial diversity (Dinan and Cryan 2015), rendering the host more susceptible to infection and consequently negatively affecting innate immune function (Patterson et al. 2014). Additionally, recent studies have identified that subject biological age but not chronological age correlate with a decrease in stool microbial diversity (Maffei et al. 2017), that is, pathological aging is associated with a narrowing in microbial diversity while healthy aging correlates with a more diverse microbiota (Dinan and Cryan 2017).Fecal calprotectin—A recent study carried out on 22 Alzheimer's patients by Leblhuber et al. (2015) showed that almost three-quarters of AD patients presented fecal calprotectin concentrations higher than normal (>50 mg/kg). This is interpreted to be a sign of gastrointestinal permeability/leaky gut, where fecal calprotectin would have translocated from the gut into the circulation via disturbed intestinal barrier function. Calprotectin is heterodimer formed by pro-inflammatory proteins S100A8 and S100A9. The latter has been established as a biomarker for the diagnosis and progression of AD and dementia (Horvath et al. 2016).Zonulin and nutrient status—Zonulin is a physiological modulator of intercellular tight junction function and thus a regulator of gut permeability (Fasano 2012). Exposure to air pollution (Calderon-Garciduenas et al. 2015) as well as microbial dysbiosis, high-fructose and high-fat dietary patterns, and nutritional deficiencies, for example, vitamin D, vitamin A, and zinc, are also factors known to affect gastrointestinal permeability (Teixeira et al. 2012).
Identified potential biomarkers may predict primary nonresponse to infliximab in patients with ulcerative colitis
Published in Autoimmunity, 2022
Jixiang Zhang, Xiaohan Wu, Shuchun Wei, Chuan Liu, Xiaoli Wang, Weiguo Dong
Calprotectin comprises two monomers in mammals, S100A8 and S100A9, and belongs to the calcium-binding S100 leukocyte protein family [23, 24]. An increasing number of studies have confirmed that calprotectin, especially faecal calprotectin, is closely associated with the occurrence and development of UC. The S100A8/S100A9 complex not only stimulates and enhances the activation of immune cells but also orchestrates an inflammatory response [25, 26]. TNFα has been shown to work synergistically with S100A8/A9 in inflammatory responses by up-regulating the expression of S100A8/A9 and S100A8/A9, which in turn up-regulates TNFα expression in a functional feedback loop that represents a self-sustaining inflammatory loop. In our study, we found that in the colon tissues of UC patients with primary nonresponse to infliximab, the expressions of S100A8 and S100A9 were up-regulated. Based on previous reports and our findings, we speculate that while TNFα and S100A8/A9 as the pro-inflammatory factors were remarkably upregulated, the antagonistic effect of infliximab on TNFα was offset by the induction effect of S100A8/A9 leading to primary nonresponse to infliximab.
S100A9 as a novel diagnostic and prognostic biomarker in human gastric cancer
Published in Scandinavian Journal of Gastroenterology, 2020
Zhanwei Zhao, Chaojun Zhang, Qingchuan Zhao
S100A9 is a calcium-binding protein. Recently, S100A9 was revealed as an oncogene in various cancers. For example, a recent study reported that S100A9 expression was significantly higher in lung cancer patients than in healthy volunteers and may serve as a biomarker for lung cancer diagnosis or prognosis [4]. Zhou et al. found that the serum levels of S100A9 in colorectal cancer patients were significantly lower after surgery than before surgery and that S100A9 levels could serve as diagnostic biomarkers of colorectal cancer [5]. However, the role of S100A9 in the carcinogenesis and prognosis of GC is poorly understood because of limited studies and inconsistent results. Choi et al. [6] identified S100A9 as a negative regulator of lymph node metastasis in GC, but both Kwon et al. [7] and Yong and Moon [8] found that S100A9 promoted the invasion and migration of GC cells.
Identification of differentially expressed proteins associated with recurrence in ovarian endometriotic cysts
Published in Systems Biology in Reproductive Medicine, 2020
Genhai Zhu, Jiao Kong, Xinhui Fu, Fujin Liu, Haiyan Huang, Lan Hong, Kang Wang
S100 calcium-binding protein A8 (S100A8) and S100 calcium-binding protein A9 (S100A9) are both important members of the calcium-binding protein S100 family, and often bind to form heterodimers needed for various functions (Argyris et al. 2018). S100A8 and S100A9 function in regulating cell migration, promoting the production of proinflammatory factors, and as adhesion molecules (Cluzeau et al. 2017). They also mediate inflammatory reactions and modulate the amount and extent of a certain immune response. S100A8 is often included in tumor-related studies (Austermann et al. 2017; Wu et al. 2018). S100A8 and S100A9 are thought to play similar roles in the pathogenesis of endometriosis, despite the fact that no reports concerning their roles in endometriosis have been published. Adhesion, epithelial metaplasia, and immune factors exert critical function in the pathogenesis of endometriosis, and it can be speculated that S100A8 and S100A9 proteins may affect these factors to regulate the occurrence and recurrence of endometriosis (Moris et al. 2016). In addition, our results showed that the S100A8 and S100A9 proteins were expressed at different levels in normal ovarian tissues when compared to ovarian endometriotic cyst tissues, and were obviously up-regulated in ovarian endometriotic cysts. Consequently, S100A8 and S100A9 may be involved in the recurrence mechanism of ovarian endometriotic cysts, and represent new markers for the evaluation of disease severity, the effect of treatment, and disease recurrence.