Objectives Circular RNAs (circRNAs) are RNA transcripts that belong to non‐coding RNAs (ncRNAs), whose implication in human cancers has been recently demonstrated. However, the specific role of multiple circRNAs in breast cancer remains unidentified. Materials and methods Microarray analysis and bioinformatics analysis were applied to select circRNA and miRNA, respectively. The loop structure of circ‐TFF1 was confirmed using RNase R treatment, divergent primer PCR and Sanger sequencing. qRT‐PCR and Western blot were employed for gene expressions. In vitro and in vivo experiments were conducted to assess the function of circ‐TFF1 in biological processes in breast cancer cells. FISH and subcellular separation indicated circ‐TFF1 cellular distribution. Luciferase reporter and RIP assays and Pearson's correlation analysis were performed to evaluate relationships between genes. Results Circ‐TFF1 and TFF1 were both upregulated and positively associated with each other in breast cancer. Knockdown of circ‐TFF1 hindered breast cancer cell proliferation, migration, invasion and EMT in vitro and controlled tumour growth in vivo. Circ‐TFF1 acted as a ceRNA of TFF1 by sponging miR‐326, and its contribution to breast cancer progression was mediated by miR‐326/TFF1 axis. Conclusions Circ‐TFF1 is a facilitator in breast cancer relying on TFF1 by absorbing miR‐326, providing a novel promising target for BC treatment.

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Krüppel‐like transcription factor (KLF) family is involved in tumorigenesis in different types of cancer. However, the importance of KLF family in gastric cancer is unclear. Here, we examined KLF gene expression in five paired liver metastases and primary gastric cancer tissues by RT‐PCR, and immunohistochemistry was used to study KLF8 expression in 206 gastric cancer samples. The impact of KLF8 expression on glycolysis, an altered energy metabolism that characterizes cancer cells, was evaluated. KLF8 showed the highest up‐regulation in liver metastases compared with primary tumours among all KLF members. Higher KLF8 expression associated with larger tumour size ( P < 0.001), advanced T stage ( P = 0.003) and N stage ( P < 0.001). High KLF8 expression implied shorter survival outcome in both TCGA and validation cohort ( P < 0.05). Silencing KLF8 expression impaired the glycolysis rate of gastric cancer cells in vitro. Moreover, high KLF8 expression positively associated with SUVmax in patient samples. KLF8 activated the GLUT4 promoter activity in a dose‐dependent manner ( P < 0.05). Importantly, KLF8 and GLUT4 showed consistent expression patterns in gastric cancer tissues. These findings suggest that KLF8 modulates glycolysis by targeting GLUT4 and could serve as a novel biomarker for survival and potential therapeutic target in gastric cancer.