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  • Title: MALAT1/miR-124/Capn4 axis regulates proliferation, invasion and EMT in nasopharyngeal carcinoma cells.
    Author: Shi B, Wang Y, Yin F.
    Journal: Cancer Biol Ther; 2017 Oct 03; 18(10):792-800. PubMed ID: 28857668.
    Abstract:
    BACKGROUND: Long non-coding RNA MALAT1 (Metastasis-associated lung Adenocarcinoma transcript-1) has been demonstrated to play a critical role in the regulation of cancer progression and metastasis. However, little is known about MALAT1 in nasopharyngeal carcinoma (NPC) pathogenesis and progression. METHODS: Quantitative real-time PCR (qRT-PCR) was conducted to measure the expression of MALAT1, miR-124 and Capn4 mRNA in NPC cell lines. The protein level of Capn4 was examined by western blot analysis. Cell proliferation was detected by MTT assay, trypan blue exclusion method and colony formation analysis. Cell invasion was determined by transwell chamber assay. Expression of EMT-related proteins was detected by western blot. The potential targets of MALAT1 and miR-124 were verified by target prediction and luciferase reporter assay. RESULTS: MALAT1 and Capn4 were upregulated while miR-124 expression was downregulated in NPC cell lines. MALAT1 knockdown inhibited proliferation, invasion and EMT of NPC cells. Moreover, MALAT1 improved Capn4 expression by sponging miR-124. MALAT1 upregulation abated miR-124-induced repression on NPC cell proliferation, invasion and EMT. Furthermore, Capn4 overexpression reversed the inhibitory effect of MALAT1 silencing on proliferation, invasion and EMT of NPC cells. CONCLUSION: MALAT1 promoted proliferation, invasion and EMT of NPC cells through de-repressing Capn4 by sponging miR-124. The present study revealed a novel MALAT1/miR-124/Capn4 regulatory axis in NPC, contributing to a better understanding of the NPC pathogenesis and providing a promising therapeutic target for NPC therapy.
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