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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

Component Drug category Effect on HOTAIR Comment References
Calycosin Phytostrogen isoflavon Down-regulation Induces apoptosis by down-regulating phosphorylation of HOTAIR upstream target, Akt [116]
Genistein Soy isofalvone Down-regulation Represses HOTAIR as well as NF-κB and Akt signalling pathways, while it overexpresses miR-141 [116, 119]
BIO Genistein nano-suspension Down-regulation Inhibits GSK3β and induces β-Catenin signalling, leading to down-regulation of HOTAIR [37]
Delphinidin-3-glucoside  Anthocyanidin Down-regulation Induces apoptosis via activation of IRF1 and repression of Akt [53]
Imatinib + Lapatinib Anti-neoplastic agent Down-regulation Synergistically supress β-Catenin and subsequently HOTAIR expression [117]
BML-284 Wnt agonist Down-regulation Induces Wnt/β-Catenin signalling pathway and repression of HOTAIR [37]
Bisphenol-A estrogenic endocrine disrupting chemical Up-regulation Interferes with normal estrogen signalling pathway, leading to expression of HOTAIR by inducing the corresponding ERE promoter, in addition to particular histone modifications [95]
Diethylstilbestrol Synthetic estrogen Up-regulation Involved in normal estrogen signalling pathway and HOTAIR expression, through interaction with the corresponding ERE promoter and particular histone modifications [95]
Gemcitabine Anti-metabolite agents Up-regulation Through unknown mechanism, this agent up-regulates HOTAIR causing further malignant cell proliferation, self-renewal and migration [104]