Microglia are the resident phagocytic cells with various functions in the central nervous system, and the morphologies of microglia imply the different stages and functions. In optical nerve transection (ONT) model in the retina, the retrograde degeneration of retinal ganglion cells (RGCs) induces microglial activations to a unique morphology termed “rod” microglia. A few studies described the “rod” microglia in the cortex and retina; however, the function and origin of “rod” microglia are largely unknown. In the present study, we firstly studied the temporal appearance of “rod” microglia after ONT, and found the “rod” microglia emerge at approximately 7 days after ONT and peak during 14 to 21 days. Interestingly, the number of “rod” microglia remarkably decays after 6 weeks. Secondly, the “rod” microglia eliminate the degenerating RGC debris by phagocytosis. Moreover, we found the major source of “rod” microgliosis is local proliferation rather than the infiltration of peripheral monocytes/hematopoietic stem cells. We for the first time described the appearance of “rod” retinal microglia following optic nerve transection.

ObjectiveEVA1B, a protein coding gene, is a critical paralog of EVA1A gene. Herein, our study was conducted to investigate the role of EVA1B in colorectal cancer (CRC) progression and prognosis.MethodsPan-cancer analysis was conducted to analyze expression, genetic and epigenetic alterations, and immunological characteristics of EVA1B. Especially, immunological characteristics and mutational landscape were compared between high and low EVA1B expression groups in the combined TCGA-COAD and TCGA-READ datasets. Through random survival forest analysis, an EVA1B-derived genomic model was developed, and its prognostic value was verified in the external datasets (GSE14333, GSE39582, and GSE87211). Drug sensitivity was compared between high- and low-risk subpopulations. A nomogram was conducted through integrating independent factors.ResultsEVA1B expression presented a remarkable upregulation in most cancer types, especially CRC. EVA1B expression was significantly correlated to DNA methyltransferases, DNA mismatch repair genes, m6A regulators, TMB, and MSI across pan-cancer. High EVA1B expression indicated an undesirable CRC patients’ prognosis. Additionally, its upregulation was correlated to enhanced immune cell infiltration, increased stromal and immune activation, and elevated activities of cancer immunity cycle. Higher frequencies of amplification and deletion were investigated in high EVA1B expression subpopulation. Following verification, the EVA1B-derived genomic model reliably predicted patients’ prognosis and drug responses. The nomogram (age, stage, EVA1B-derived risk score) was conducted to quantify an individual’s survival probability. Furthermore, our experimental validation based on immunohistochemistry indicated that EVA1B overexpression is correlated with CRC tumorigenesis and poor outcomes in our CRC patients’ cohort.ConclusionCollectively, our findings provided valuable resource for guiding the mechanisms and therapeutic analysis of EVA1B in CRC.

Hepatocellular carcinoma (HCC) is one of the malignancies with an extremely inferior prognosis in the abdominal cavity, making it essential to develop more effective biomarkers for HCC. Although GNG5 has been linked to increased patient survival in a variety of human malignancies, no evidence has been found for its involvement in the development of HCC yet. Our study first analyzed the expression and prognosis of GNG5 in HCC using The Cancer Genome Atlas database (TCGA database) with the Gene Expression Omnibus database (GEO database) and found that GNG5 has a potential oncogenic role. Based on survival analysis, the clinical importance and prognostic value of the GNG5 gene were studied. Relying on tumor Immune Estimation Resource database (TIMER database), we analyzed the correlation between the GNG5 gene and HCC Immune infiltration cells. GNG5 expression levels were significantly higher in HCC tissues compared to normal liver tissues. HCC patients with high GNG5 expression had significantly reduced overall survival time and affected multiple immune cell infiltrates. Additionally, KEGG functional enrichment analysis indicated the PI3K-Akt signaling pathway as the most promising carcinogenic pathway associated with GNG5. This is the first comprehensive revelation of GNG5 as a possible new biological marker associated with immune infiltration in HCC. Additionally, it holds promise as an emerging target for HCC immunotherapy.