Background: Gastric cancer (GC) is one of the most common malignant tumors of the digestive system. As a hallmark of cancer, energy-related metabolic reprogramming was manipulated by various factors, including lncRNAs. It has been shown that lncRNA CCAT1 is a key regulator involved in tumor development. Nevertheless, the exact underlying molecular mechanisms by which lncRNA CCAT1 acts in GC metabolic reprogramming are yet to be elucidated. Methods: The expression of CCAT1 in GC tissues, serum, and exosome that was isolated from plasma and GC cell lines were detected by qRT-PCR. The gain and loss-function assays were performed to explore the role of CCAT1 on GC cells. Xenograft tumor formation models in nude mice were performed to estimate the proliferation of GC cells with CCAT1 stably knocking down in vivo. The proteins interacting with CCAT1 were first analyzed by online databases and further confirmed by RNA pull-down and RNA immunoprecipitation (RIP) assays. The expression of glycolytic signaling pathway-related proteins were probed using western blotting and immunohistochemistry (IHC). Results: In this study, we identified that CCAT1 was remarkably enhanced in the tissues, serum, and plasma exosomes of GC patients as well as in GC cell lines. Functional experiments showed that knockdown of CCAT1 significantly reduced the proliferation, migration and invasion of GC cells in vitro and in vivo, and also decreased glycolytic rate and the expression of glycolytic enzymes in GC cells, whereas overexpression of CCAT1 had opposing effects. Mechanically, CCAT1 interacted with PTBP1 and maintained its stability by inhibiting the ubiquitin-mediated degradation. As a critical splicing factor, PTBP1 induced a switch from PKM1 to PKM2, leading to an increase in the glycolysis of GC cells and ultimately promoting GC progression. Conclusions: Our study exhibited that CCAT1 contributed to GC proliferation, migration and invasion via PTBP1 / glycolysis axis, making it a potential biomarker and therapeutic target in GC patients.