Purpose: Colon cancer (CC) is a leading cause of cancer-related deaths worldwide. This study aimed to clarify the effect of long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on CC progression and the potential mechanism.
Methods: CC cell lines HCT116 and HT29 were selected for functional analysis. The expression of MALAT1, microRNA (miR)-101-3p , and stanniocalcin 1 (STC1) in CC tissues and cells were measured by quantitative reverse transcription PCR (qRT-PCR). Cell proliferation, apoptosis, migration and invasion were measured by Cell Counting Kit-8 (CCK-8), flow cytometry, wound scratch and transwell assay, respectively. The target relationships (MALAT1 and miR-101-3p, miR-101-3p  and STC1) were validated by dual-luciferase reporter and RNA pull-down assay.
Results: The expression of MALAT1 was elevated in CC tissues compared with adjacent normal tissues and was associated with lymph node metastasis, depth of invasion and tumor-node-metastasis (TNM) stage. Up-regulation of MALAT1 promoted the proliferation, migration, and invasion and inhibited the apoptosis of CC cells; while MALAT1 knockdown exhibited opposite results. MiR-101-3p  was a target of MALAT1, which was negatively regulated by MALAT1. Silencing of miR-101-3p reverses the anti-tumor effect of MALAT1 knockdown on CC cells. STC1 was a target of miR-101-3p , which was negatively regulated by miR-101-3p . Silencing of STC1 reverses the tumor promoting effects of MALAT1 up-regulation and miR-101-3p down-regulation on CC cells.
Conclusion: MALAT1 may function as an oncogene in CC progression by affecting the miR-101-3p /STC1 axis, providing a hopeful therapeutic option for CC.
Keywords: colon cancer, MALAT1, miR-101-3p , proliferation, apoptosis, migration, invasion