Baoyuan Shi1, Yandan Wang1, Fengfang Yin2. 1. a Department of Otorhinolaryngology , Huaihe Hospital of Henan University , Henan , Kaifeng , China. 2. b Department of Otorhinolaryngology , the First Affiliated Hospital of Henan University , Henan , Kaifeng , China.
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.
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.
Authors: King Chi Chan; Lai Sheung Chan; Joseph Chok Yan Ip; Carman Lo; Timothy Tak Chun Yip; Roger Kai Cheong Ngan; Ricky Ngok Shun Wong; Kwok Wai Lo; Wai Tong Ng; Anne Wing Mui Lee; George Sai Wah Tsao; Michael Kahn; Maria Li Lung; Nai Ki Mak Journal: Sci Rep Date: 2015-04-21 Impact factor: 4.379
Authors: Xiao Hong Peng; Hao Ran Huang; Juan Lu; Xiong Liu; Fei Peng Zhao; Bao Zhang; Shao Xiong Lin; Lu Wang; Huai Hong Chen; Xia Xu; Fan Wang; Xiang Ping Li Journal: Mol Cancer Date: 2014-08-07 Impact factor: 27.401