The RNA methyltransferase NSUN2 has been involved in the cell proliferation and senescence, and is upregulated in various types of cancers. However, the role and potential mechanism of NSUN2 in gastric cancer remains to be determined. Our study showed that NSUN2 was significantly upregulated in gastric cancers, compared to adjacent normal gastric tissues. Moreover, NSUN2 could promote gastric cancer cell proliferation both in vitro and in vivo. Further study demonstrated that CDKN1C (p57 Kip2) was the potential downstream gene of regulated by NSUN2 in gastric cancer. NSUN2 could promote gastric cancer cell proliferation through repressing p57 Kip2 in an m 5 C-dependent manner. Our findings suggested that NSUN2 acted as an oncogene through promoting gastric cancer development by repressing p57 Kip2 in an m 5 C-dependent manner, which may provide a novel therapeutic target against gastric cancer.

Podoplanin, lymphatic vessel endothelial hyaluronic acid receptor-1, prospero-related homeobox-1 and vascular endothelial growth factor receptor 3 have been demonstrated to have crucial roles in the development of the lymphatic system and lymphangiogenesis process by combining with their corresponding receptors. Thus, the four markers have been widely used in labelling lymphatic vessels for the detection of lymphangiogenesis and lymphatic vessel invasion. Numerous authors have aimed to identify the roles of these four markers in the lymphatic system and the mechanisms have been partly clarified at the molecular level. The aim of the present review was to comprehensively clarify the characteristics and latent action modes of the four markers in order to determine which is the best one for the detection of lymphangiogenesis and lymphatic vessel invasion.

Abstract. The human histamine receptor H1 (HRH1) gene is located on chromosome 3p25 and encodes for a 487 amino acid G protein-coupled receptor (GPCR) with a long third intracellular loop (IL3). The HRH1 predominantly couples to Gα q/11 proteins, leading to the activation of phospholipase C (PLC) and subsequent release of the second messengers inositol trisphosphate (IP 3 ) and diacylglycerol (DAG) followed by the activation of PKC and the release of [Ca 2+ ] i . In the present study, we identified HRH1 genes from 14 vertebrate genomes and found that HRH1 exists in all types of vertebrates including fish, amphibians, birds and mammals. We identified 88 SNPs including 4 available alleles disrupting an existing exonic splicing enhancer and 84 SNPs causing missense mutation, which may impact the effect of histamine on the HRH1 protein. We found that the human HRH1 gene was expressed in many tissues or organs, and predominant expression of HRH1 was shown in the bone marrow, whole blood, lymph node, thymus, brain, cerebellum, retina, spinal cord, heart, smooth muscle, skeletal muscle, small intestine, colon, adipocytes, kidney, liver, lung, pancreas, thyroid salivary gland, skin, ovary, uterus, placenta, prostate and testis. When searched in the PrognoScan database, human HRH1 was also found to be expressed in bladder cancer, blood cancer, brain cancer, breast cancer, colorectal cancer, eye cancer, head and neck cancer, lung cancer, ovarian cancer, skin cancer and soft tissue cancer tissues. The relationship between the expression of HRH1 and prognosis was found to vary in different types of cancers, even in the same cancer from different databases. This implies that the function of HRH1 in these tumors may be multidimensional. GR, STAT5A and c-Myb regulatory transcription factor binding sites were identified in the HRH1 gene upstream (promoter) region, which may be involved in the effect of HRH1 in tumors.

AIM: To investigate the relationship between inactivation of p16 gene and gastric carcinoma, and the mechanism of inactivation of p16 gene in gastric carcinogenesis. METHODS:40 fresh tumor tissue specimens were taken from primary gastric cancer patients. Expression of P16 protein was detected by immunohistochemical method. Deletion and point mutation of p16 gene were analyzed by polymerase chain reaction (PCR) and DNA sequencing, respectively. RESULTS:The frequency of loss of P16 protein expression in the gastric cancer tissue, adjacent nontumor tissue, and distal normal tissue was 77.5 % (31/40), 55.0 % (22/40), and 17.5 % (7/40), respectively (P<0.005). Homozygous deletion of exon 1 and exon 3 was observed in two and three cases, respectively, giving an overall frequency of homozygous deletion of 12.5 %. All five cases had diffuse type gastric carcinoma. No p16 gene point mutation was detected. CONCLUSION: