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Fig. 1 | Clinical Epigenetics

Fig. 1

From: SEPT9_v2, frequently silenced by promoter hypermethylation, exerts anti-tumor functions through inactivation of Wnt/β-catenin signaling pathway via miR92b-3p/FZD10 in nasopharyngeal carcinoma cells

Fig. 1

The expression levels and promoter methylation levels of SEPT9_v2 in NPC tissues, HNSC tissues, and cell lines. NM tissues and HNSN tissues were used as controls. a The promoter methylation level of SEPT9_v2 in 71 NPC tissues was significantly higher in comparison with 8 normal nasal mucosal tissues by MSP. b SEPT9_v2 expression in 9 human nasopharyngeal carcinomas and 9 NM tissues detected by qPCR. c SEPT9_v2 promoter methylation in 20 paired HNSC and HNSN tissue samples from the MethHC database. d SEPT9_v2 promoter methylation in 516 HNSC samples and 50 HNSN samples. e SEPT9_v2 mRNA expression and methylation status in HONE1 and HNE1 cell lines were detected by RT-PCR and MSP analysis. SEPT9_v2 was downregulated and hypermethylated in HONE1 and HNE1 cell lines. GAPDH was used as an input control. GAPDH was used as an input control. f qPCR detected SEPT9_v2 mRNA expression in HONE1 and HNE1 cell lines treated with Aza (A) without or with TSA (T). Error bars mean standard deviation (SD); values are presented as the mean ± SD of at least three independent experiments. Aza, 5-aza-2′-deoxycytidine; HNSC, head and neck squamous cell carcinomas; HNSN, head and neck squamous epithelium; MSP, methylation-specific polymerase chain reaction; M, methylated; NPC, nasopharyngeal carcinoma; NM, normal nasal mucosal; SD, standard deviation; U, unmethylated; RT-PCR, reverse transcription polymerase chain reaction. *p < 0.05, **p < 0.01, ***p < 0.001

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