2015
DOI: 10.1016/j.bbrc.2014.12.114
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17β-Estradiol regulates cell proliferation, colony formation, migration, invasion and promotes apoptosis by upregulating miR-9 and thus degrades MALAT-1 in osteosarcoma cell MG-63 in an estrogen receptor-independent manner

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Cited by 66 publications
(54 citation statements)
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“…highly similar to what has been previously reported for complex diseases; gene promoters and HC islands were under-represented and intragenic regions and LC CpGs overrepresented among DMRs compared to the whole array distribution of the CpG sites (Irizarry et al, 2009;Nilsson et al, 2014;Ollikainen et al, 2015;Yang et al, 2015). Hence, HRT seems to affect DNA methylation in similar genomic regions as reported for common multifactorial diseases.…”
Section: Discussionsupporting
confidence: 87%
See 1 more Smart Citation
“…highly similar to what has been previously reported for complex diseases; gene promoters and HC islands were under-represented and intragenic regions and LC CpGs overrepresented among DMRs compared to the whole array distribution of the CpG sites (Irizarry et al, 2009;Nilsson et al, 2014;Ollikainen et al, 2015;Yang et al, 2015). Hence, HRT seems to affect DNA methylation in similar genomic regions as reported for common multifactorial diseases.…”
Section: Discussionsupporting
confidence: 87%
“…Both of these larger entities are highly relevant for HRT. Estrogen has been shown to regulate cell proliferation and apoptosis (Fang et al, 2015), and to increase cognitive abilities and In order to go beyond only reporting associations on genome-wide DNA methylation we investigated the potential biological relevance of the identified within-pair methylation differences by exploring whether any of the genes with DMRs are differentially expressed.…”
Section: Discussionmentioning
confidence: 99%
“…In breast cancer cells that express estrogen receptor-, 17-estradiol treatment negatively regulates MALAT1 transcription, leading to the inhibition of cell proliferation, migration, and invasion [41,42]. In esophageal cancer, SRY-box 17…”
Section: Transcriptional Regulation Of Malat1mentioning
confidence: 99%
“…[16][17][18] LncRNA MALAT1 might function as an oncogene through controlling alternative splicing process in breast cancer, influencing the expression of N-cadherin and E-cadherin in bladder cancer, combining with a multifunctional RNA-binding protein in colorectal cancer (CRC) and osteosarcoma. [19][20][21][22] LncRNA HOX antisense intergenic RNA (HOTAIR)…”
Section: Introductionmentioning
confidence: 99%