Osteosarcoma (OS) is a primary malignant bone tumor most commonly affecting children and adolescents and is characterized by loss of differentiation. Bone morphogenetic protein/retinoic acid inducible neural-specific 3 (BRINP3) has been reported to regulate the differentiation of osteoblasts. However, the role that BRINP3 plays in the progression of osteosarcoma remains unknown. We found in this study that BRINP3 was highly expressed in 64.13% of human osteosarcoma tissues and it was associated with histological grade, tumor recurrence, and poor clinical prognosis of osteosarcoma. In vitro, downregulation of BRINP3 was able to inhibit the proliferation and invasion of osteosarcoma cell lines. Furthermore, BRINP3 interacted with microtubule-associated protein 4 (MAP4) at the protein level, and overexpression of MAP4 could partially reverse the inhibitory effect of downregulated BRINP3 on the proliferation and invasion of osteosarcoma cells, which indicates that downregulation of BRINP3 might suppress the proliferation and invasion of osteosarcoma cells by inhibiting MAP4 expression. Overall, our results demonstrate that BRINP3 functions as an oncogene within osteosarcoma through MAP4 and could therefore be used as a potential biomarker for osteosarcoma diagnostics and therapeutics.
Purpose Although papillary renal cell carcinoma (PRCC) has a relatively favorable prognosis, a small number of patients with lymph node or distant metastasis have a poor prognosis. Owing to the complex typing and heterogeneity of PRCC, it remains difficult to provide risk stratification. The objective of our research was to identify potential markers of PRCC prognosis. Methods We performed proteomics and bioinformatics analyses on six pairs of formalin‐fixed paraffin‐embedded tumor and paired normal tissue samples. The Cancer Genome Atlas (TCGA) data were used to analyze the prognostic value of differentially expressed proteins (DEPs) in PRCC. We verified the expression of the major biomarker through immunohistochemistry (IHC) in 91 PRCC tumor specimens. Results Proteomic analysis revealed 1544 DEPs between tumor and paired normal tissues. PRCC transcriptomic data from the TCGA database revealed that compared to non‐tumor tissues, the expression of high‐mobility group protein A2 (HMGA2) was upregulated in tumor tissues, and patients with high HMGA2 expression exhibited shorter overall survival times. HMGA2 was associated with PRCC tissue subtype and higher cell pleomorphism. Both TCGA and IHC results showed that HMGA2 expression was associated with lymph node metastasis and clinical stage. Conclusion HMGA2 was positively correlated with malignant progression and could be a valuable novel prognostic biomarker for PRCC risk stratification.
Background: Giant cell tumor of the bone (GCTB), an intermediate locally aggressive neoplasm that frequently involves the epiphyseal region of the long bones. GCTB of the distal phalanx and soft-tissue recurrences are extremely rare. Little is known about the cellular and molecular differences between GCTB of the long bones and rare sites. Methods:We employed single-cell RNA sequencing to elucidate the transcriptional profiles of 28,992 cells originating from patients afflicted with GCTB in the femur, distal phalanx, and soft-tissue relapse. To confirm the critical findings, we subjected the paraffin sections of GCTB to immunohistochemical staining.Results: Our study revealed that GCTBs in rare sites display distinct immune subtypes and antigen presentation gene signatures. We observed minimal lymphocyte infiltration in GCTBs of the phalanx. Further analyses demonstrated that the transforming growth factor-β pathway and profibrotic proteins were significantly upregulated in phalanx lesions. In contrast, GCTB cells from soft-tissue recurrence exhibited discernible chondrocyte characteristics but presented lower antigen-presenting ability compared to those from femur lesions. Notably, we identified an immunosuppressive subset of mast cells in the soft-tissue recurrence. The secretion of proangiogenic and immunosuppressive factors from these mast cells suggests their potential role in the formation of vascular-rich and immunosuppressive niches in recurrent lesions.
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