The competing endogenous RNA (ceRNA) hypothesis was introduced as a previously unrecognized gene regulatory layer. This is a recently discovered hypothesis about how mRNAs, pseudogene transcripts, long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs) regulate post-transcriptional expression by sharing common microRNA response elements (MREs) to compete for the binding of microRNAs (miRNAs) and inhibiting normal miRNA targeting activity on mRNA. Previous study have found that ceRNAs are key regulators in many biological processes such as cell cycle, tumor initiation and progression and found to be involved in several diseases, especially in tumor. Tumor is a kind of serious disease with high death rate. Recently, there is no effective therapy for Tumor. The mechanism of many tumors has not yet been fully elucidated. It has been proved that a number of ceRNAs identified as aberrantly expressed during tumor development. It is vital to understand how ceRNA works in tumor progression and to find a new way to cure those corresponding disease. This review introduces the mechanism of ceRNA hypothesis, focus on the history of the ceRNA hypothesis, the important pathophysiological roles of ceRNAs in tumor and the latest findings about how ceRNA works in gastric cancer, lung cancer, endometrial cancer, breast cancer, liver cancer, colorectal cancer and melanoma.