Fig. 6: FOXD2-AS1 conferred cancer stemness and chemotherapy resistance in laryngeal cancer through STAT3 activation. | Cell Death & Disease

Fig. 6: FOXD2-AS1 conferred cancer stemness and chemotherapy resistance in laryngeal cancer through STAT3 activation.

From: Long noncoding RNA FOXD2-AS1 enhances chemotherapeutic resistance of laryngeal squamous cell carcinoma via STAT3 activation

Fig. 6

a Representative micrographs and quantification of tumor spheres formed by FOXD2-AS1-overexpressing laryngeal cancer cells treated with vehicle or STAT3 inhibitor stattic. Histograms showed the mean number of spheres formed by the indicated cells. b Real-time PCR analysis of OCT4, SOX2, and NANOG expression in indicated cells that under stattic treatment and control cells. Expression levels were normalized to GAPDH. c Viability of indicated cells after 24 h cisplatin treatment or treating with cisplatin plus stattic, implicating that stattic-abolished FOXD2-AS1 induced cisplatin resistance of laryngeal cancer cells. d Colony formation of FOXD2-AS1-overexpressing cells with indicated treatment. e, f The effect of STAT3 inhibition by stattic on tumor formation of FOXD2-AS1-overexpressing laryngeal cancer cells during cisplatin treatment (n = 6/group). Stattic treatment significantly rescued the sensitivity to cisplatin in FOXD2-AS1-overexpressing cells. g IHC staining of Ki67 and TUNEL staining were performed to verified the proliferation and anti-apoptosis potential of FOXD2-AS1-overexpressing cells accompanied with indicated treatment. *P < 0.05, **P < 0.01, and ***P < 0.001.

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