Study on <em>CCDC69</em> interfering with the prognosis of patients with breast cancer through PPAR signal pathway

Abstract

Coiled-coil domain-containing protein 69 (CCDC69) is a novel gene and limited knowledge in known in breast cancer. In the present study, we aimed to explore the relationship between CCDC69 and breast cancer, demonstrate the clinicopathological significance and prognostic role of CCDC69 in breast cancer, and analyze the possible mechanism of CCDC69 affecting the prognosis of breast cancer. First, from GEO database, TIMER, GEPIA, and OncoLnc, we select CCDC69 as the potential gene which closely involved in breast cancer progression. Next, by real-time PCR detection, the expression of CCDC69 in breast cancer tissue was notably lower than that in normal breast tissues (p=0.0002). In addition, our immunohistochemistry (IHC) indicated that the positive expression rate of CCDC69 in the triple-negative breast cancer (TNBC) was lower than that in the non-TNBC (p=0.0362), and it was negatively correlated with the expression of Ki67 (p=0.001). Further enrichment analysis of CCDC69 and the similar genes performed on FunRich3.1.3 revealed that these genes were significantly associated with fat differentiation, and most of them were related to peroxisome proliferator-activated receptor (PPAR) signal pathway. Collectively, our findings suggest that CCDC69 is down regulated in breast cancer tissue especially in TNBC which has higher malignant grade and poorer clinical prognosis.

Susceptibility Loci for Type 2 Diabetes in the Ethnically Endogamous Indian Sindhi Population: A Pooled Blood Genome-Wide Association Study

“…Published evidence implicated these 18 genes directly through population studies (GBP6, GSTO1, HHIPL1, INTS10, RGS16 and RNU6-679P), indirectly through association with other metabolic conditions (CCDC69, DNAH2, GALNT17, HERC5, KIF5C, MARCH2 and PRDM14) or through association with complications of T2D (CASC15, CCDC107, MIR147A, PFKFB3 and RNF166). Detailed annotation of the published literature in this regard is provided in Supplementary Table S3 ) [ 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 ]. From the remaining genes identified to be significantly associated with T2D in this study, there were two open reading frames, three long intergenic non-coding elements and a pseudogene.…”