The prognostic role of γδ T cells in colorectal cancer based on nomogram.

OBJECTIVE: The aim of the present study was to explore the prognostic role of γδ T cells in colorectal cancer, and establish a nomogram for predicting the survival of the patients. METHODS: Immunohistochemistry was performed to analyze the infiltration degree of γδ T cells in tumor and normal tissues of colorectal cancer. The relationship between γδ T cells infiltration in tumor tissues and the prognosis of patients with colorectal cancer were determined by Cox regression analysis and survival analysis. R software was used to establish and verify a nomogram for predicting the prognosis of patients with colorectal cancer. RESULTS: The degree of γδ T cell infiltration in tumor tissues and normal tissues of CRC was not different (t = 0.35, P = 0.73). However, the infiltration of γδ T cell was related to the survival status of the patients (x2 = 4.88, P = 0.03). Besides, the infiltrating degree of γδ T cells in tumor tissue was obviously related to the prognostic improvement of the patients with colorectal cancer (log-rank P = 0.02) and could reflect the benefit of adjuvant chemotherapy. The nomogram based on tumor diameter, tumor location, AJCC stage, chemotherapy, serum CEA level and γδ T cell infiltration was established and could provide a reference for predicting the survival of colorectal cancer patients. CONCLUSION: γδ T cell infiltration degree in tumor tissue was an important factor to improve the outcome of patients with colorectal cancer, and can predict the benefit of adjuvant chemotherapy.

Downregulation of the FBXO43 gene inhibits tumor growth in human breast cancer by limiting its interaction with PCNA.

BACKGROUND: The function and regulatory mechanism of FBXO43 in breast cancer (BC) are still unclear. Here, we intended to determine the role and mechanism of FBXO43 in BC. METHODS: FBXO43 expression in BC was evaluated by analysis of The Cancer Genome Atlas (TCGA). RT-qPCR and western blotting were utilized to detect FBXO43 expression in BC cell lines. Lentivirus was applied to downregulate FBXO43 in human BC cells. Proliferation assays were performed to evaluate the proliferative ability of BC cells. The apoptosis and cell cycle analysis of BC cells were analyzed by flow cytometry. Cell migration and invasion were investigated via Transwell assays. The function of FBXO43 in vivo was evaluated by constructing a xenograft mouse model. The proteins that might interact with FBXO43 in BC were identified by mass spectrometry, bioinformatics analysis, and co-immunoprecipitation (Co-IP) assays. Finally, rescue experiments were conducted to validate the recovery effects of the proteins interacting with FBXO43. RESULTS: FBXO43 was highly expressed in BC and was significantly downregulated after FBXO43 knockdown. The proliferation, migration, and invasion of BC cells were inhibited, and cell apoptosis was induced by FBXO43 knockdown. In addition, an in vivo experiment indicated that FBXO43 knockdown could inhibit the cell growth of BC. The results of the Co-IP assay showed that FBXO43 interacted with PCNA. Further rescue experiments confirmed that overexpression of PCNA significantly reversed the effects of FBXO43 knockdown on BC cells. CONCLUSION: Downregulation of FBXO43 inhibits the tumor growth of BC by limiting its interaction with PCNA. FBXO43 might be a new potential oncogene and a therapeutic target for BC.