lncRNA FAM230B is highly expressed in colorectal cancer and suppresses the maturation of miR-1182 to increase cell proliferation.

Abstract

Long non-coding RNA FAM230B and microRNA (miR-1182) have been characterized as critical players in cancer biology, while their roles in colorectal cancer (CRC) are unclear. We predicted that they could interact with each other and therefore explored the interaction between them in CRC. CRC and paired non-tumor tissue samples were collected from 60 CRC patients, and the expression of FAM230B and miR-1182 (premature and mature) in these samples was analyzed with RT-qPCR. The direct interaction between FAM230B and premature miR-1182 was analyzed with RNA-RNA pull-down assay, and the subcellular location of FAM230B was detected with subcellular fractionation assay. The interaction between FAM230B and miR-1182 was explored with overexpression assay, and their roles in regulating CRC cell proliferation, viability, and colony formation were assessed by BrdU assay, MTT assay, and colony formation assay, respectively. We found that FAM230B and premature miR-1182 were highly upregulated in CRC, while mature miR-1182 was downregulated in CRC. FAM230B was detected in both nucleus and cytoplasm, and it directly interacted with miR-1182. FAM230B overexpression increased the expression levels of premature miR-1182 but decreased the expression levels of mature miR-1182 in CRC cells. FAM230B promoted CRC cell proliferation, increased cell viability, accelerated colony formation, and suppressed the role of miR-1182 in inhibiting CRC cell proliferation. In conclusion, FAM230B is upregulated in CRC and it suppresses the maturation of miR-1182 to promote tumor growth.