Down-regulation of Sp1 suppresses cell proliferation, clonogenicity and the expressions of stem cell markers in nasopharyngeal carcinoma

• DOI: 10.1186/s12967-014-0222-1
• Publication Date: 2014-08-06T10:41:06Z
• Authors: Jing-Ping Zhang; Hua Zhang; Hong-Bo Wang; Yan-Xian Li; Gui-Hong Liu; Shan Xing; Man-Zhi Li; Mu-Sheng Zeng
• Keywords: Sp1 transcription factor; BMI1; MTT assay

Transcription factor Sp1 is multifaceted, with the ability to function as an oncogene or a tumor suppressor, depending on cellular context. We previously reported that required for transcriptional activation of key oncogenes in nasopharyngeal carcinoma (NPC), including B-lymphoma mouse Moloney leukemia virus insertion region 1 (Bmi1) and centromere protein H (CENPH), but role its underlying mechanisms NPC remained largely unexplored. The objective this study was investigate verify clinical significance potential therapeutic target NPC. levels normal primary epithelial cells (NPECs) cell lines were analyzed by Quantitative Real-time RT-PCR (qRT-PCR) Western blot. location expression tissues detected immunohistochemistry staining (IHC). effect knockdown proliferation, clonogenicity, anchorage-independent growth stem-cell like phenotype evaluated MTT, flow cytometry, clonogenicity analysis sphere formation assay. mRNA elevated than NPECs. Higher found advanced stage (P = 0.00036). Either inhibition activity mithramycin A, FDA-approved chemotherapeutic anticancer drug silencing two distinct siRNA against suppressed cells. Mechanism revealed may suppress through inducing p27 p21, impairing expressions critical stem transcription factors (SCTFs), Bmi1, c-Myc KLF4 enriched significantly inhibited cells, suggesting serve appealing