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Table 2 Effect of some chemical drugs on the expression of HOTAIR

From: The emerging role of the long non-coding RNA HOTAIR in breast cancer development and treatment

ComponentDrug categoryEffect on HOTAIRCommentReferences
CalycosinPhytostrogen isoflavonDown-regulationInduces apoptosis by down-regulating phosphorylation of HOTAIR upstream target, Akt[116]
GenisteinSoy isofalvoneDown-regulationRepresses HOTAIR as well as NF-κB and Akt signalling pathways, while it overexpresses miR-141[116, 119]
BIOGenistein nano-suspensionDown-regulationInhibits GSK3β and induces β-Catenin signalling, leading to down-regulation of HOTAIR[37]
Delphinidin-3-glucoside AnthocyanidinDown-regulationInduces apoptosis via activation of IRF1 and repression of Akt[53]
Imatinib + LapatinibAnti-neoplastic agentDown-regulationSynergistically supress β-Catenin and subsequently HOTAIR expression[117]
BML-284Wnt agonistDown-regulationInduces Wnt/β-Catenin signalling pathway and repression of HOTAIR[37]
Bisphenol-Aestrogenic endocrine disrupting chemicalUp-regulationInterferes with normal estrogen signalling pathway, leading to expression of HOTAIR by inducing the corresponding ERE promoter, in addition to particular histone modifications[95]
DiethylstilbestrolSynthetic estrogenUp-regulationInvolved in normal estrogen signalling pathway and HOTAIR expression, through interaction with the corresponding ERE promoter and particular histone modifications[95]
GemcitabineAnti-metabolite agentsUp-regulationThrough unknown mechanism, this agent up-regulates HOTAIR causing further malignant cell proliferation, self-renewal and migration[104]