The promotive role of lncRNA MIR205HG in proliferation, invasion, and migration of melanoma cells via the JMJD2C/ALKBH5 axis

被引:5
作者
Liu, Yujing [1 ]
Wang, Suihai [2 ]
Wei, Shanshan [1 ]
Qiu, Xianwen [1 ]
Mei, Yijie [1 ]
Yan, Lu [1 ]
机构
[1] Southern Med Univ, Dept Dermatol, Zhujiang Hosp, Guangzhou, Peoples R China
[2] Southern Med Univ, Sch Biotechnol, Guangzhou, Peoples R China
基金
中国国家自然科学基金;
关键词
LONG NONCODING RNA; HISTONE DEMETHYLASE; CANCER; PROGRESSION; CERNA;
D O I
10.1371/journal.pone.0290986
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Melanoma is a highly malignant skin cancer. This study aimed to investigate the role of long non-coding RNA MIR205 host gene (lncRNA MIR205HG) in proliferation, invasion, and migration of melanoma cells via jumonji domain containing 2C (JMJD2C) and ALKB homolog 5 (ALKBH5). Real-time quantitative polymerase chain reaction or Western blot assay showed that MIR205HG, JMJD2C, and ALKBH5 were increased in melanoma cell lines. Cell counting kit-8, colony formation, and Transwell assays showed that silencing MIR205HG inhibited proliferation, invasion, and migration of melanoma cells. RNA immunoprecipitation, actinomycin D treatment, and chromatin immunoprecipitation showed that MIR205HG may bind to human antigen R (HuR, ELAVL1) and stabilized JMJD2C expression, and JMJD2C may increase the enrichment of H3K9me3 in the ALKBH5 promotor region to promote ALKBH5 transcription. The tumor xenograft assay based on subcutaneous injection of sh-MIR205HG-treated melanoma cells showed that silencing MIR205HG suppressed tumor growth and reduced Ki67 positive rate by inactivating the JMJD2C/ALKBH5 axis. Generally, MIR205HG facilitated proliferation, invasion, and migration of melanoma cells through HuR-mediated stabilization of JMJD2C and increasing ALKBH5 transcription by erasing H3K9me3.
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页数:17
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