METHODS: Eight electronic databases (Web of Science, PubMed, ScienceDirect, American Psychological Association PsycNet, Cochrane Library, Scopus, Embase, and Ovid) were searched for the study. Articles published from January 1 to December 31, 2022, were considered for this review. A random-effects meta-analysis and between-study heterogeneity analysis were conducted using Comprehensive Meta-Analysis V3.0 software.
RESULTS: We identified 7829 articles of which 28 met the full inclusion criteria and were included in the systematic review and analyses. Our pooled analysis suggested that participants with MCI can be differentiated from HC by significant P200, P300, and N200 latencies. The P100 and P300 amplitudes were significantly smaller in participants with MCI when compared with those in the HCs, and the patients with MCI showed increased N200 amplitudes. Our findings provide new insights into potential electrophysiological biomarkers for diagnosing MCI.
METHODS: The TCGA portal was employed in this investigation to find APOC1 expression in CRC. Its correlation with other genes and clinicopathological data was examined using the UALCAN database. To validate APOC1's cellular location, the Human Protein was employed. In order to forecast the relationship between APOC1 expression and prognosis in CRC patients, the Kaplan-Meier plotter database was used. TISIDB was also employed to evaluate the connection between immune responses and APOC1 expression in CRC. The interactions of APOC1 with other proteins were predicted using STRING. In order to understand the factors that contribute to liver metastasis from CRC, single-cell RNA sequencing (scRNA-seq) was done on one patient who had the disease. This procedure included sampling preoperative blood and the main colorectal cancer tissues, surrounding colorectal cancer normal tissues, liver metastatic cancer tissues, and normal liver tissues. Finally, an in vitro knockdown method was used to assess how APOC1 expression in tumor-associated macrophages (TAMs) affected CRC cancer cell growth and migration.
RESULTS: When compared to paracancerous tissues, APOC1 expression was considerably higher in CRC tissues. The clinicopathological stage and the prognosis of CRC patients had a positive correlation with APOC1 upregulation and a negative correlation, respectively. APOC1 proteins are mostly found in cell cytosols where they may interact with APOE, RAB42, and TREM2. APOC1 was also discovered to have a substantial relationship with immunoinhibitors (CD274, IDO1, and IL10) and immunostimulators (PVR, CD86, and ICOS). According to the results of scRNA-seq, we found that TAMs of CRC tissues had considerably more APOC1 than other cell groups. The proliferation and migration of CRC cells were impeded in vitro by APOC1 knockdown in TAMs.
CONCLUSION: Based on scRNA-seq research, the current study shows that APOC1 was overexpressed in TAMs from CRC tissues. By inhibiting APOC1 in TAMs, CRC progression was reduced in vitro, offering a new tactic and giving CRC patients fresh hope.