Fig. 1

BisPhenol A, diethylstilbesterol, and IRF1 promote the overexpression of HOTAIR by binding to the corresponding gene promoter elements. Bisphenol A and diethylstilbesterol independently interact with estrogen receptors in the cytoplasm, translocate into the nucleus, associate with the methyl transferases MLL1 and MLL3, bind to the estrogen receptor elements ERE1 and ERE3, and then activate the overexpression of HOTAIR. IRF1 binds to the downstream sequence in between 53–64 and 136–148 within the promoter region and activates the overexpression of HOTAIR. P65, which is an important component of the NF-kB signaling pathway, directly binds to the sequence between − 443 and − 475 within the promoter element and regulates the expression of HOTAIR. Myocardin Related Transcription Factor(MRTF-A) binds to the CArG box located in the HOTAIR promoter and facilitates the association between SRF1 and RNA POL II, which is involved in the expression of HOTAIR. Transcription factor c-Myc binds specifically to the E-box sequence within the HOTAIR promoter region and increases its expression. FOXA1 and FOXM1 interact with the HOXC locus positioned adjacent to the HOTAIR gene promoter and regulates its expression LncRNA DRHC suppresses HOTAIR expression and inhibits the proliferation of triple negative BC cells. SMAD2/3/4 interacts with the promoter region of HOTAIR between − 386 and − 398 and between − 440 and − 452 to facilitate the transcription of HOTAIR, while MJD6 induces the expression of HOTAIR by directly binding to its promoter in the − 13 to −103 region