Document Type : Original Article
Department of Gastroenterology, Suzhou Science and Technology Town Hospital of Nanjing Medical University, Suzhou, Jiangsu, China
Reportedly, long non-coding RNA (lncRNA) cancer susceptibility candidate 2 (CASC2) is involved in
regulating colorectal cancer (CRC) progression. However, the function and detailed downstream mechanism of CASC2
in CRC progression are not fully elucidated. The aim of the study was to investigate the potential function and molecular
mechanism of CASC2 in CRC progression.
Materials and Methods:
In this experimental study, quantitative real-time polymerase chain reaction (qRT-PCR) was
adopted to probe CASC2, microRNA-18a-5p (miR-18a-5p) and B cell translocation gene 3 (BTG3) mRNA expression
in CRC tissues and cell lines. After CASC2 was overexpressed in Colo-678 and HCT116 cell lines, methylthiazol
tetrazolium (MTT) and 5-bromo-2’-deoxyuridine (BrdU) assays were employed to examine the proliferation of CRC cells.
Transwell migration and invasion assays were executed to evaluate the metastatic potential of CRC cells. The targeting
relationships among CASC2, miR-18a-5p and BTG3 were validated by dual luciferase reporter gene assay. Western
blot assay was applied to examine the regulatory effects of CASC2 and miR-18a-5p on BTG3 protein expression.
CASC2 was decreased in CRC tissues and cell lines, and its low expression in CRC tissues was associated
with larger tumor size and lymph node metastasis. CASC2 overexpression restrained proliferative, migrative and
invasive capabilities of CRC cells. CASC2 could function as a molecular sponge for miR-18a-5p and repress the
expression of miR-18a-5p. Furthermore, the inhibitory effects of CASC2 on the malignant phenotypes of CRC cells was
counteracted by miR-18a-5p mimics. Additionally, CASC2 could positively regulate BTG3 expression via suppressing
CASC2 inhibits CRC development by suppressing miR-18a-5p and raising BTG3 expression.