Long non-coding RNA EGFR-AS1 in colorectal cancer: potential role in tumorigenesis and survival via miRNA-133b sponge and EGFR/STAT3 axis regulation

ABSTRACT

Background

Colorectal cancer is one of the most common cancers worldwide and a major cause of cancer-related death. Thus molecular biomarkers for colorectal cancer have been proposed. The role of long non-coding RNA EGFR-AS1 in colorectal cancer is still unclear. We aimed to evaluate its expression in different stages of colorectal cancer and determine any possible role in regulating the miR‑133b/EGFR/STAT3 signalling pathway.

Materials and Methods

The relative expression of EGFR-AS1 and miR‑133b were evaluated by quantitative real-time RT-transcription PCR in 130 colorectal cancer samples and 30 normal tissues. EGFR expression was assessed using immunohistochemistry. Furthermore, levels of p-EGFR, p-STAT3, and apoptotic proteins were determined by ELISA.

Results

Both EGFR-AS1 and EGFR overexpression were positively linked with colorectal cancer status (both p < 0.01), grade (both p < 0.01), and metastasis (P < 0.01 and p = 0.019 respectively). EGFR-AS1 and miR-133b were significantly inversely correlated (P < 0.01). Low expression of miR-133b was inversely associated with overexpressed EGFR and increased p-STAT3 levels. EGFR-AS1 was an independent prognostic factor for survival of colorectal cancer patients (P < 0.01, HR 2.06; 95% CI 1.32–3.19) where low EGFR-AS1 expression was associated with higher survival rate (p = 0.003).

Conclusion

EGFR-AS1 may have a role in colorectal cancer by regulation of miR‑133b/EGFR/STAT3 signalling. It may be a potential biomarker for early diagnosis and predicting the survival rate of colorectal cancer.

KEYWORDS:

• Colorectal cancer
• epidermal growth factor receptor-antisense RNA 1
• microRNA‑133b
• Epidermal growth factor receptor
• signal Transducer and Transcription Activator 3

Acknowledgements

The authors would like to express our deepest thanks for all patients participating in the current study.

Disclosure statement

The authors declare no potential conflict of interest concerning this work.

Additional information

Funding

This work did not receive funding from any organizations.