Abstract
Accumulating evidence suggested that lncRNA MALAT1 plays critical roles in the commencement and progression of malignant cancers. Nevertheless, the function of MALAT1 in colorectal cancer (CRC) remains largely unknown. In the present study, we reported that MALAT1 expression is significantly upregulated in CRC and correlated with advanced TNM stage, lymph node metastasis, and worse prognosis in patients. Functional assays revealed that MALAT1 knockdown reduced CRC cell growth and invasion abilities in vitro. Mechanistically, we discovered that MALAT1 may serve as a competing endogenous RNA (ceRNA) to miR-508-5p in CRC progression. Bioinformatics analysis and luciferase assays confirmed that RAB14 acts as a target of miR-508-5p. In addition, downregulation of RAB14 reduced the progression of CRC. Collectively, our findings indicated that MALAT1 could promote CRC progress by sponging miR-508-5p and enhancing RAB14 expression, which provides a therapeutic target in CRC treatment.
Highlights
Colorectal cancer (CRC) is one of the most prevalent malignancies worldwide [1, 2]
Accumulating data shows that Long noncoding RNAs (lncRNAs) play critical roles in CRC development [18]
A number of studies have shown that Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) might be a biomarker in CRC progression
Summary
Colorectal cancer (CRC) is one of the most prevalent malignancies worldwide [1, 2]. the prognosis has ameliorated due to advances in both diagnosis and treatment of CRC, the molecular mechanisms that lead to the development of the tumor remain unclear [3, 4]. Accumulating data indicated that aberrant lncRNA expression has important functions in diverse biological processes, including growth, differentiation, autophagy, and metastasis [6, 7]. Zhu et al [8] demonstrated that lncRNA ANCR decreased osteoblast differentiation by regulating the EZH2/Runx axis. Sun et al [10] demonstrated that lncRNA HOXA11-AS encouraged gastric cancer cell growth and invasion by regulating DNMT1, LSD1, and PRC2 expression. Wu et al [13] discovered that MALAT1 encourages gallbladder cancer cell proliferation and invasion by regulating the ERK/MAPK axis. Xie et al [14] demonstrated that MALAT1 increases bladder cancer cell invasion ability by regulating miR-125b expression. The mechanism of MALAT1 in CRC advancement is still uncertain
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