Abstract
Colon cancer is one of the major causes of cancer-related deaths worldwide. Long non-coding RNA (lncRNA) LINC01123 has been suggested to act as an oncogene in non-small cell lung cancer and a prognostic signature in head and neck squamous cell carcinoma. However, its role in colon cancer remains obscure. From TCGA database, LINC01123 was observed to be up-regulated in colon adenocarcinoma (COAD). Subsequently, the up-regulated LINC01123 was also detected in colon cancer cells. Functionally, LINC01123 could enhance cell proliferation, migration, invasion and angiogenesis. Moreover, the chemoresistance of colon cancer cells was verified to be promoted by LINC01123. Afterward, LINC01123 was found to bind with Ago2 and miR-34c-5p. Besides, miR-34c-5p was confirmed to inhibit the cellular process and chemoresistance of colon cancer cells. Then, VEGFA was disclosed to coexist with LINC01123 and miR-34c-5p in RNA-induced silencing complex. And TCGA database suggested that its expression was correlated with different stages of COAD. Moreover, it was uncovered that VEGFA could bind with miR-34c-5p and its expression positively correlated with LINC01123 expression. Finally, LINC01123 was proofed to regulate colon cancer progression and cells chemoresistance via VEGFA. In conclusion, LINC01123/miR-34c-5p/VEGFA axis promotes colon cancer malignancy and cells chemoresistance.
Highlights
Featured with late tumor occurrence, rapid development, and metachronous metastasis, colon cancer is the third leading cause of cancer-related deaths worldwide [1]
We first employed The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases to analyze the expression of LINC01123 in colon adenocarcinoma (COAD)
The results revealed that LINC01123 was up-regulated in COAD (Figure 1A)
Summary
Featured with late tumor occurrence, rapid development, and metachronous metastasis, colon cancer is the third leading cause of cancer-related deaths worldwide [1]. The transformation from normal colonic mucosa to colon cancer involves a progression of accumulating genetic changes [5]. LncRNAs are incapable of encoding proteins but could take part in the regulation of gene expression at various levels [8]. LncRNAs could epigenetically regulate the expression of genes by recruiting EZH2. At the post-transcriptional level, lncRNAs could interact with RNA binding proteins to mediate the stability of mRNAs. Besides, lncRNAs could antagonize the availability of microRNA (miRNA) to free the messenger RNA (mRNA) from the regulation of miRNA [9]. A group of lncRNAs have been discovered to participate in the regulation of colon cancer progression, such as B3GALT5-AS1 [10], SNHG15 [11], HOXB-AS3 [12] and CCAT2 [13]. LINC01123 has been revealed to be transcriptionally activated by c-Myc and could act as a molecular
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