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It has been hypothesized that cancer stem-like cells are responsible fortumor recurrence following chemotherapy. Evidence on the mechanisms through whichdrug-resistant stem-like cells recapitulate the tumor mass has not been definitivelyreported. Based on this information, we investigated the enrichment ability ofa population of stem-like cells following treatment with cisplatin in human A549cells and focused on the molecular mechanisms regulating the self-renewal of stem-likecells. A population of stem-like cells was enriched following cisplatin treatmentand was defined phenotypically and functionally based on the expression of certainstem cell markers, sphere-forming ability, multipotent differentiation and inductionof xenograft tumors in vivo. For various types of differentiated cells, Bmi1 hasbeen reported to be important for cell proliferation and for the self-renewalof stem cells. The high expression of Bmi1 in cisplatin-enriched stem-like cellswas shown using Q-PCR and western blotting; therefore, the role of Bmi1 was investigatedin cisplatin-enriched stem-like cells by infecting cisplatin-enriched stem-likecells with Bmi1-targeted RNAi lentiviruses. Cell proliferation, tumor sphere formationand xenograft formation was reduced following knockdown of Bmi1. Based on ourresults, we propose that, after cisplatin treatment, Bmi1 is required for theself-renewal of stem-like cells that are important for the expansion of the stem-likecell pool in human A549 cells and that targeting Bmi1 slows down the formationof tumors in vivo.

shRNA targeting Bmi1 impedes the self-renewal of cisplatin-enriched stem-like cells in human A549 cells