miR-9 modulates the expression of interferon-regulated genes and MHC class I molecules in human nasopharyngeal carcinoma cells

Journal Article · Fri Feb 15 04:00:00 EST 2013 · Biochemical and Biophysical Research Communications

DOI:https://doi.org/10.1016/J.BBRC.2012.12.097· OSTI ID:22239502

Gao, Fei; Zhao, Zun-Lan; Zhao, Wen-Tao; Fan, Quan-Rong; Wang, Sheng-Chun; Li, Jing; Zhang, Yu-Qing; Shi, Jun-Wen; Lin, Xiao-Lin; Yang, Sheng; Xie, Rao-Ying ^[1]; Liu, Wei ^[2]; Zhang, Ting-Ting; Sun, Yong-Liang ^[1]; Xu, Kang ^[3]; Yao, Kai-Tai ^[1]; Xiao, Dong ^[1]

---

1. Cancer Research Institute, Southern Medical University, Guangzhou 510515 (China)
2. Institute of Comparative Medicine and Laboratory Animal Center, Southern Medical University, Guangzhou 510515 (China)
3. Department of General Surgery, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou 510120 (China)

Highlights: ► miR-9 can negatively or positively modulate interferon-induced gene expression. ► miR-9 can up-regulate major histocompatibility complex class I molecule expression. ► miR-9 can down-regulate the expression of interleukin-related genes. -- Abstract: The functions of miR-9 in some cancers are recently implicated in regulating proliferation, epithelial–mesenchymal transition (EMT), invasion and metastasis, apoptosis, and tumor angiogenesis, etc. miR-9 is commonly down-regulated in nasopharyngeal carcinoma (NPC), but the exact roles of miR-9 dysregulation in the pathogenesis of NPC remains unclear. Therefore, we firstly used miR-9-expressing CNE2 cells to determine the effects of miR-9 overexpression on global gene expression profile by microarray analysis. Microarray-based gene expression data unexpectedly demonstrated a significant number of up- or down-regulated immune- and inflammation-related genes, including many well-known interferon (IFN)-induced genes (e.g., IFI44L, PSMB8, IRF5, PSMB10, IFI27, PSB9{sub H}UMAN, IFIT2, TRAIL, IFIT1, PSB8{sub H}UMAN, IRF1, B2M and GBP1), major histocompatibility complex (MHC) class I molecules (e.g., HLA-B, HLA-C, HLA-F and HLA-H) and interleukin (IL)-related genes (e.g., IL20RB, GALT, IL7, IL1B, IL11, IL1F8, IL1A, IL6 and IL7R), which was confirmed by qRT-PCR. Moreover, the overexpression of miR-9 with the miRNA mimics significantly up- or down-regulated the expression of above-mentioned IFN-inducible genes, MHC class I molecules and IL-related genes; on the contrary, miR-9 inhibition by anti-miR-9 inhibitor in CNE2 and 5–8F cells correspondingly decreased or increased the aforementioned immune- and inflammation-related genes. Taken together, these findings demonstrate, for the first time, that miR-9 can modulate the expression of IFN-induced genes and MHC class I molecules in human cancer cells, suggesting a novel role of miR-9 in linking inflammation and cancer, which remains to be fully characterized.

• OSTI ID: 22239502
• Journal Information: Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 3 Vol. 431; ISSN 0006-291X; ISSN BBRCA9
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
ANGIOGENESIS
APOPTOSIS
CARCINOMAS
GENES
HISTOCOMPATIBILITY COMPLEX
INFLAMMATION
INHIBITION
INTERFERON
METASTASES
MOLECULES
PATHOGENESIS
POLYMERASE CHAIN REACTION