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CpG hypomethylation at proximal promoter and 5'UTR along with IL6 signaling loop associates with MYD88 upregulation in epithelial ovarian cancer

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机构： [1]Department Gynecological Oncology, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, Affiliated Cancer Hospital of University of Electronic Science and Technology of China, No. 55, Section 4, South People’s Road, Chengdu 610041, China. [2]Department of Ultrasound, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, Affiliated Cancer Hospital of University of Electronic Science and Technology of China, Chengdu 610041, China. [3]Biochemistry and Molecular Biology, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, Affiliated Cancer Hospital of University of Electronic Science and Technology of China, No. 55, Section 4, South People’s Road, Chengdu 610041, China.

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关键词： Epithelial ovarian cancer Myeloid differentiation factor 88 Interleukin-6 Specificity protein 1 Interferon regulatory factor 1 CpG methylation

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MYD88 is an IL-6 primary response gene and, its upregulation of expression has been shown to be a poor prognostic factor in epithelial ovarian cancer (EOC). We investigated the effects of CpG methylation at the proximal promoter/5'UTR and IL-6/SP1/IRF1 signaling on upregulation of MYD88 and prognosis in EOC. We assessed CpG methylation at the proximal promoter/5'UTR of MYD88 using bisulfite sequencing/PCR in 103 EOC patients, 28 normal ovarian tissues and two EOC cell lines with differential expression of MYD88 and identified the impact of the level of CpG methylation on MYD88 upregulation by SP1/IRF1 with knockdown or blockade of IL-6. The proximal promoter/5'UTR of MYD88 was significantly hypomethylated in 75 EOC tissues compared to 28 normal ovarian tissues (P < 0.001). CpG hypomethylation was relevant to MYD88 upregulation in 75 EOC cases (R2 = 0.4376; P < 0.001). Of them, 38 cases with m5CpGlow/MYD88high/IL-6high were associated with reduced progression-free/overall survival compared to 37 cases with m5CpGhigh/MYD88low/IL-6low (P < 0.01). Knockdown of IL-6 or blockade with IL-6 receptor McAb attenuated MYD88 upregulation by SP1/IRF1 signaling in EOC cells with MYD88high (P < 0.001). In conclusion, CpG hypomethylation at the proximal promoter/5'UTR contributes to MYD88 upregulation in EOC via IL-6/SP1/IRF1 pathway.© 2024. The Author(s).

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大类 | 2 区综合性期刊

小类 | 2 区综合性期刊

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Q1 MULTIDISCIPLINARY SCIENCES

影响因子： 3.8 最新[2023版] 4.3 最新五年平均 3.8 出版当年[2023版] 0 出版当年五年平均 3.8 出版前一年[2023版]

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第一作者机构： [1]Department Gynecological Oncology, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, Affiliated Cancer Hospital of University of Electronic Science and Technology of China, No. 55, Section 4, South People’s Road, Chengdu 610041, China.

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