Ttc39c is a potential target for the treatment of lung cancer

Abstract

Background The novel TTC gene, tetratricopeptide repeat domain 39 C (Ttc39c), mainly mediates the interaction between proteins. It is involved in the progression of various tumors. In this study, we determined the effect of Ttc39c on lung adenocarcinoma and found that it might be used as a potential intervention target. Methods We performed a difference analysis of Ttc39c samples from the TCGA database. Transwell experiments were conducted to determine the ability of cell metastasis. Celigo and MTT assays were performed to determine the effect of Ttc39c gene subtraction on cell proliferation. FACS was performed to determine the effect of Ttc39c gene subtraction on apoptosis. Clone-formation experiments were conducted to determine the effect of Ttc39c gene subtraction on cloning ability. Transcriptomics, proteomics, and metabolomics were used to elucidate the enrichment pathway of the Ttc39c gene in the progression of lung adenocarcinoma. Results The expression of Ttc39c increased significantly in lung adenocarcinoma. The proliferation, metastasis, and cloning ability of human lung cancer cells were inhibited, while the apoptosis of cells increased significantly after the depletion of Ttc39c. Our results based on the transcriptomics, proteomics, and metabolomics analyses indicated that Ttc39c might be involved in the progression of lung adenocarcinoma (LUAD) mainly through the metabolic pathway and the p53 pathway. Conclusion To summarize, Ttc39c strongly regulates the proliferation and metastasis of lung adenocarcinoma cells. The main pathways involved in Ttc39c in lung adenocarcinoma include the energy metabolism and p53 pathways.

Tissue-resident memory T cell signatures from single-cell analysis associated with better melanoma prognosis

“…Many of these T RM signature genes are related to tumor progression or immune pathways, such as the BCAS4, 38 CAMK4, 39 GIMAP2, 40 , 41 IFITM, 42 KPNA2, 43 MKI67, 44 NCCRP1, 45 NCL, 46 PRKAR2B, 47 TTC39C. 48

Figure 5 Stratified survival analysis of the 22-gene risk score model Kaplan-Meier survival analysis for the patients in independent datasets by the 22-gene risk score model. (A) Development of a T RM risk score for GLIOMA by LASSO Cox regression analysis.

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“…Many of these T RM signature genes play important roles in the T cell activating, antigen-presenting, tumor progression, and immune response, such as the BCAS4, CAMK4, GIMAP2, IFITM1, KPNA2, MKI67, NCCRP1, NCL, PRKAR2B, and TTC39C. 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 Low-risk patients could with high T RM cell infiltration, and our results also showed that the T cell (such as the memory T cells, Th1 cells, Th2 cells, and Th17 cells), immune checkpoint, and other immune regulation-related pathways were significantly up-regulated in the low-risk or high T RM infiltration patients, which could be further investigated to understand the interplay between T RM and the TIME.…”