Cell proliferation was significantly impeded and cancer cells exhibited an enhanced stem‐like phenotype when cytoplasmic CCAT2 was present in vitro within the luminal subtype of MCF‐7 or T47D cancer of the breast cells. The stimulation of miR‐221‐p27 signaling resulted in the suppression of tumor development in vivo. On the other hand, OCT4‐PG1 expression increased and cancer cell stemness was stimulated as a consequence of overexpressed CCAT2 in the nucleus. Here, POU5F1 is linked to neoplasm.