Abstract
Simple SummaryLong noncoding RNA dysfunction is crucial for colorectal carcinoma (CRC) development. Whether the dysfunction of LOC441461, a novel lncRNA, can regulate cancer-related signaling pathways in cancer progression remains unclear. Here, we uncover the oncogenic role of LOC441461 in colon cancer cell growth and motility and identify a novel mechanism for LOC441461 knockdown-induced suppression of cancer motility through modulating Ras homolog family member A (RhoA)/Rho-associated protein kinase (ROCK) activity. This is the first report that LOC441461 knockdown impairs cell cycle progression and accelerates the apoptosis of colon cancer cells following chemotherapy drug treatment. The results suggest that LOC441461 expression confers drug sensitivity in colon cancer by inducing apoptosis. Our findings offer new insight into LOC441461 regulation and provide an application for colon cancer therapy in the future.Colorectal carcinoma (CRC) is one of the most prevalent cancers worldwide and has a high mortality rate. Long noncoding RNAs (lncRNAs) have been noted to play critical roles in cell growth; cell apoptosis; and metastasis in CRC. This study determined that LOC441461 expression was significantly higher in CRC tissues than in adjacent normal mucosa. Pathway enrichment analysis of LOC441461-coexpressed genes revealed that LOC441461 was involved in biological functions related to cancer cell growth and motility. Knockdown of the LOC441461 expression significantly suppressed colon cancer cell growth by impairing cell cycle progression and inducing cell apoptosis. Furthermore, significantly higher LOC441461 expression was discovered in primary colon tumors and metastatic liver tumors than in the corresponding normal mucosa, and LOC441461 knockdown was noted to suppress colon cancer cell motility. Knockdown of LOC441461 expression suppressed the phosphorylation of MLC and LIMK1 through the inhibition of RhoA/ROCK signaling. Overall, LOC441461 was discovered to play an oncogenic role in CRC cell growth and motility through RhoA/ROCK signaling. Our findings provide new insights into the regulation of lncRNAs and their application in the treatment of colon cancer
Highlights
Colorectal carcinoma (CRC) is one of the most prevalent cancers worldwide and has a high mortality rate [1,2]
Our findings revealed that LOC441461 has a novel oncogenic role in regulating CRC cell growth and migration through modulating RhoA/ROCK
We determined the long noncoding RNAs (lncRNAs) profile of CRC by using the microarray approach and identified several lncRNAs that were deregulated in CRC tissues compared with adjacent normal tissues [7]
Summary
Colorectal carcinoma (CRC) is one of the most prevalent cancers worldwide and has a high mortality rate [1,2]. The mortality rate of CRC has gradually decreased, its overall survival rate remains poor when the cancer is advanced. Determining the molecular mechanism of colon cancer genesis and metastasis is a research topic of interest. The identification and elucidation of the dysregulated genes involved in colon cancer progression and the development of an excellent biomarker to aid early diagnosis or act as a potential therapeutic target would benefit patients with CRC. Noncoding RNAs (ncRNAs) are functional RNA transcripts that lack protein translation ability, and ncRNA dysfunction plays a crucial role in human cancer progression [4,5]. On the basis of their size, ncRNAs can be classified as small ncRNAs (microRNAs) or long noncoding RNAs (lncRNAs)
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