Research on the genetic mechanisms underlying cancer formation and metastasis has focused on protein-coding exons, which comprise less than 2% of the human genome. The remaining 98% is less well understood. Recent research has revealed that the noncoding genome is pervasively transcribed and that noncoding RNA genes have key roles in cancer. Pseudogenes are a type of noncoding gene that are mutated copies of protein-coding genes and are thought to be functionless evolutionary relics due to their inability to encode functional proteins. Atlases of human gene expression have determined that pseudogenes are widely transcribed in highly-specific patterns in normal tissues and tumours (Kalyana-Sundaram et al., Cell, 2012; Han et al., Nature Communications, 2014). Pseudogenes can regulate their parental counterparts through noncoding mechanisms, including as antisense RNAs, microRNA decoys and piRNA hosts (reviewed in Poliseno et al., Frontiers in Medicine, 2015). To identify functional pseudogenes that regulate their parent genes we analysed RNA-seq data from tens of thousands of normal tissues and tumours. Inversely correlated expression may be indicative of a functional relationship between gene-pseudogene pairs and precludes mis-mapping artefacts due to sequence similarity with the parent gene. We identified hundreds of candidate pseudogenes whose expression is significantly anticorrelated with their parent genes. Several of these anticorrelated pseudogenes are copies of key oncogenes and tumour suppressors and are thus intriguing targets for functional studies. An overexpression screen of anti-correlated pseudogenes revealed that the pseudogene PDCL3P4 suppresses its parent gene PDCL3. PDCL3P4 overexpression disrupts key genes in the c-jun, MAPK and NFKB signalling pathways and inhibits p15 and p21 expression, promoting cell cycle progression. Conversely ablation of PDCL3P4 by CRISPR-Cas9 genome-engineering decreases proliferation. This study identifies that pseudogenes can play critical roles in the regulation of cell division and may be important factors in tumorigenesis.