Fig. 7: Schematic illustration of the possible regulatory mechanisms in this study.

ER deficiency promoted TFAP-2-inducible LINC00511 expression by enhancing the occupancy efficiency of TFAP-2 at specific promoter regions. The ER-negative-associated LINC00511, which was mainly located in the nucleus, repressed the expression of CDKN1B via interacting with EZH2 to recruit PRC2 to mediate histone methylation, contributing to the G1/S transition to sustain cell proliferation