Background This study attempted to verify the potential of KCNJ14 as a biomarker in colorectal cancer (CRC). Methods Data on transcriptomics and DNA methylation and the clinical information of CRC patients were downloaded from The Cancer Genome Atlas and Gene Expression Omnibus databases. Biological information analysis methods were conducted to determine the role of KCNJ14 in the prognosis, diagnosis, immune cell infiltration, and regulation mechanism of CRC patients. The effect of KCNJ14 on the proliferation and migration of HCT116 and SW480 CRC cell lines was verified by in vitro experiments (MTT, colony-forming, wound healing, and transwell assays). Western blotting was performed to detect the effect of KCNJ14 on the levels of mTOR signalling pathway-related proteins. Results KCNJ14 expression was remarkably increased in CRC tissues and cell lines, which reduced the overall survival time of patients. KCNJ14 mRNA was negatively regulated by its methylation site cg17660703, which can also endanger the prognosis of patients with CRC. Functional enrichment analysis suggested that KCNJ14 is involved in the mTOR, NOD-like receptor, and VEGF signalling pathways. KCNJ14 expression was positively correlated with the number of CD4 + T cells and negatively correlated with that of CD8 + T cells in the immune microenvironment. KCNJ14 knockdown significantly reduced not only the proliferation and migration of CRC cell lines but also the levels of mTOR signalling pathway-related proteins. Conclusions This study not only increases the molecular understanding of KCNJ14 but also provides a potentially valuable biological target for the treatment of colorectal cancer.

As important regulatory molecules, LncRNAs play an important role in regulating the pathological progress of malignant tumor. However, the effect of LncRNA-HOXD-AS2 on the prognosis of colorectal cancer and its regulatory mechanism has not been confirmed. Therefore, this study obtained the transcriptome data and clinicopathological characteristics of colorectal cancer from TCGA database to predict the impact of HOXD-AS2 on the prognosis of patients and its regulatory mechanism. It was found that the high expression of HOXD-AS2 had a positive relationship with the expression of pathological T and tumor stages and can significantly reduce the overall survival of patients and have diagnostic value for prognosis. Subsequent, GSEA prediction found that HOXD-AS2 could promote the activation of TGF-β signaling pathway. MTT assay and Ki67 staining assay confirmed that HOXD-AS2 knockdown could significantly inhibit the proliferation ability of the SW480 and SW620 cells of colorectal cancer. Transwell assay and wound healing assay demonstrated that knockdown of HOXD-AS2 could significantly inhibit the invasion and migration of SW480 and SW620 cells. Finally, Western blotting showed that the knockdown of HOXD-AS2 could significantly reduce the expression level of key proteins of TGF-β signaling pathway. Collectively, this study revealed the regulatory effect of HOXD-AS2 on the pathological mechanism of colorectal cancer for the first time, and broadened the molecular function of HOXD-AS2. The increased expression of HOXD-AS2 in colorectal cancer can be used as a biological target for the biological treatment of colorectal cancer.