OBJECTIVE: Long non-coding RNAs (lncRNAs) are emerging as key molecules in 
cancers, yet their potential molecular mechanisms are not well understood. The 
objective of this study is to examine the expression and functions of lncRNAs in 
the development of colorectal cancer (CRC).
METHODS: LncRNA expression profiling of CRC, adenoma and normal colorectal 
tissues was performed to identify tumour-related lncRNAs involved in colorectal 
malignant transformation. Then, we used quantitative reverse transcription PCR 
assays to measure the tumour-related lncRNA and to assess its association with 
survival and response to adjuvant chemotherapy in 252 patients with CRC. The 
mechanisms of CCAL function and regulation in CRC were examined using molecular 
biological methods.
RESULTS: We identified colorectal cancer-associated lncRNA (CCAL) as a key 
regulator of CRC progression. Patients whose tumours had high CCAL expression 
had a shorter overall survival and a worse response to adjuvant chemotherapy 
than patients whose tumours had low CCAL expression. CCAL promoted CRC 
progression by targeting activator protein 2α (AP-2α), which in turn activated 
Wnt/β-catenin pathway. CCAL induced multidrug resistance (MDR) through 
activating Wnt/β-catenin signalling by suppressing AP-2α and further 
upregulating MDR1/P-gp expression. In addition, we found that histone H3 
methylation and deacetylases contributed to the upregulation of CCAL in CRC.
CONCLUSIONS: Our results suggest that CCAL is a crucial oncogenic regulator 
involved in CRC tumorigenesis and progression.