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

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]