![]() ![]() The serum used for the experiments was collected from the remaining serum of the standard biochemical assays.īlood from mice (C57BL/6, 3–6 months old and 20–24 months old) was collected from the retroorbital plexus. Serum samples were collected from February to November 2022 from tumor patients newly diagnosed with breast cancer, cervical cancer, colon cancer, esophageal carcinoma, gastric carcinoma, glioma, liver cancer, lung cancer, pancreatic cancer, prostate cancer, rectal cancer, renal carcinoma or thyroid carcinoma. Human serum samples were collected from people (20–30 years old and 60–84 years old) who came to the hospital for physical examination between March 2021 and June 2022. Human serum samples and mouse serum samples ![]() In addition, we investigated the effect of sEVs on tumor cells with the aim of clarifying the link between aging and tumors at the sEV level. By comparing samples from youths and seniors, we analyzed differences in protein and sEVs. In this study, we used PBA to analyze serum sEVs from healthy individuals. Proximity-dependent barcoding assay (PBA) is a technique for detecting single sEV by profiling individual sEVs via simultaneous detection of hundreds of surface proteins. TACSTD2 is upregulated in prostate cancer cells and can be secreted into sEVs to affect receptor cell function. The B7-H3 protein is increased in sEVs released from senescent prostate cancer cells and has become a diagnostic marker for prostate cancer and a new target for immunotherapy. sEVs contain proteins and various nucleic acids, participate in substance transport and signal communication, and are involved in various physiological and pathological processes. Small extracellular vesicles (sEVs) are EVs 30–100 nm in diameter with characteristic surface proteins such as TSG101, CD81, and CD63. Senescent luminal cells highly express tumor-associated calcium signal transducer 2 (TACSTD2) and are associated with prostate cancer. Senescent fibroblasts enhance the growth of epithelial cells and promote the proliferation of breast tumor cells both in vitro and in vivo. In neurodegenerative diseases, the SASP causes astrocyte changes and promotes Alzheimer’s disease. The SASP accelerates aging, induces persistent and low-level inflammation, and increases the body’s susceptibility to disease. The SASP results in the secretion of more proteases and proinflammatory cytokines. Cellular senescence is the hallmark of aging and involves an alteration of the cellular secretome known as the senescence-associated secretory phenotype (SASP). Senescent cells do not die immediately, and they release more extracellular vesicles (EVs). The deeper manifestations of aging include cellular senescence, mitochondrial dysfunction, telomere loss, and genomic instability. Aging has been identified as a risk factor for cardiovascular diseases, neurodegenerative diseases, tumors and so on. TACSTD2 was upregulated in the serum of elderly individuals and patients with tumors, and could serve as a dual biomarker for aging and tumors.Īging is a dynamic and complex physiological process that involves a decrease in both cellular and systemic functions of the human body and an increase in the occurrence of disease. Moreover, we found that serum sEVs from the elderly (especially those with high TACSTD2 levels) promoted tumor cell (SW480, HuCCT1 and HeLa) proliferation and migration. Specifically, 9 of the 13 tumor groups exhibited elevated TACSTD2, particularly for cervical cancer, colon cancer, esophageal carcinoma, liver cancer and thyroid carcinoma. In addition, we discovered that TACSTD2 was significantly increased in samples from tumor patients and had better diagnostic value than CEA. Using ELISA, we verified the upregulation of TACSTD2 in serum from elderly human and aged mouse. Resultsīased on PBA analysis, we found that sEVs from the serum of elderly individuals highly express TACSTD2 and identified a subpopulation marked by TACSTD2. Serum samples from healthy individuals under 30 and over 60 years of age were collected to analyze differences in sEVs proteomics. Aging is a very complex physiological phenomenon, and sEVs are involved in the regulation of this mechanism.
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