Promoter Methylation-Mediated NPTX2 Silencing Promotes Tumor Growth in Human Prostate Cancer

Abstract

Neuronal pentraxin 2 (NPTX2), a secretory protein of neuronal pentraxins, was first identified in the nervous system. Several studies have shown that expression levels of NPTX2 are associated with the development of various cancers. However, whether NPTX2 is involved in prostate cancer progression is unclear. Herein, we found that NPTX2 is significantly reduced in prostate cancer tissues and cancer cell lines compared to control prostate tissues and control prostatic epithelial cell lines. Furthermore, the NPTX2 promoter is highly methylated in prostate cancer cells. Consistently, NPTX2 could be restored by treatment with the DNA methyltransferase inhibitor 5-aza-2′-deoxycytidine (decitabine, 5-AZA-dC). Overexpression of NPTX2 inhibited prostate cancer cell proliferation both in vitro and in vivo. In conclusion, our study demonstrated that NPTX2 acts as a tumor suppressor gene in prostate cancer.

Epigenetics: Mechanisms, potential roles, and therapeutic strategies in cancer progression

“…Furthermore, decitabine inhibited the proliferation-promoting effect of neuronal pentraxin 2 mediated via its methylation in prostate cancer cells. 63 As previously stated, DNA methylation drugs can modulate promoter methylation, lncRNA, and histone methylation, leading to epigenetic modifications of oncogenes and sensitizing the antitumor effects of antitumor drugs and the cytotoxic effects of immune cells.…”

Exploring Potential Epigenetic Biomarkers for Colorectal Cancer Metastasis

“…However, an aberrant increase in TSG promoter methylation results in the silencing of TSGs [98]. TSG promoter hypermethylation is widely observed in multiple cancer types, including CRC, hepatocellular carcinoma, epithelial ovarian cancer, non-small cell lung cancer, and prostate cancer [102][103][104][105]. In CRC primary tumours, the hypermethylation of bone morphogenetic protein 2 (BMP2), cyclin-dependent kinase inhibitor 2A (CDKN2A), and family with sequence similarity 134 member B (FAM134B) was associated with lymph node metastases [55][56][57].…”

ICAT promotes colorectal cancer metastasis via binding to JUP and activating the NF‐κB signaling pathway

“…Stable cell lines overexpressing the protein of interest were developed as previously described. 13,18 Lentiviruses carrying ICAT cDNA and vector control (VC) packaged by Vigene Biosciences were transfected into the SW480 cell line following the manufacturer's instructions to construct ICAT-overexpressing cell lines and VC. Stable cell lines were selected after 2 weeks of puromycin (10 μg/ml) selection and were maintained in 1 μg/ml puromycin.…”