Objective To investigate ING2 expression in normal gastric tissue,gastric carcinoma and precancerous lesions, and to explore correlation between ING2 expression and the carcinogenesis and progression of gastric carcinoma and the clinicopathological signficance as well as the correlation between ING2 and raP53 protein. Methods The expression of ING2 was measured by PV9000 two-step immunohistochemical staining. In total, 188 gastric cancer(GC), 128 matched normal gastric mucosa,35 chronic atrophic gastritis (CAG), 87 intestinal metaplasia (IM) and 36 dysplasia (DYS) samples were analyzed. Expression of mP53 was measured in 40 samples from the 188 gastric carcinomas mentioned above. Results Positive ING2 expression was significantly more frequent in CAG (74.29%) ,IM (91.95%) ,DYS (75.0%) and GCs (70.21%) than in normal gastric mucosa (36.72% ,P ＜0.05). Among GCs, ING2 expression varied by Lanren's classification. A significantly higher rate of positive ING2 expression was observed in intestinal type GCs (80. 56%) than in diffuse (64.49%) and mixed (55.56%, P ＜ 0.05) type GCs. Furthermore, positive ING2 expression was significantly more frequent in well-to-moderately differentiated adenocarcinoma(80. 60%) than in poorly differentiated adenocarcinoma (62. 62%, P ＜ 0. 05). No correlation was found between ING2 expression and mP53 expression in GC (P ＞ 0. 05). Over-expression and mislocalization of ING2 may be involved in the development of CC, especially intestinal-type GC. Further investigations are needed to explore the relevant molecular mechanism.
Key words:
Growth inhibitors; Tumor suppressor protein p53; Stomach neoplasms
Surface-enhanced Raman scattering (SERS) has been widely utilized in early detection of disease biomarkers, cell imaging, and trace contamination detection, owing to its ultra-high sensitivity. However, it is also subject to certain application restrictions in virtue of its expensive detection equipment and long-term stability of SERS-active substrate. Recently, great progress has been made in SERS technology, represented by agglomeration method. Dual readout signal detection methods are combined with SERS, including electrochemical detection, fluorescence detection, etc., establishing a new fantastic viewpoint for application of SERS. In this review, we have made a comprehensive report on development of agglomeration detection and dual-function detection methods based on SERS. The synthesis methods for plasmonic materials and mainstream SERS enhancement mechanism are also summarized. Finally, the key facing challenges are discussed and prospects are addressed.
[Objective] To investigate the effect of Suxiao Jiuxin(improving the heart function with a high speed) Pellet on the expression of SDF-1/CXCR4 in rats with atherosclerosis and to find it's mechanism of anti-atherosclerosis. [Methods] Atherosclerosis was established in rats by feeding with atherogenic diet and intraperitoneal injecting with vitamin D3 as a bolus. Sixty SD rats were randomly divid-ed into 6 groups:normal group(N) ,AS model group(Mo) ,Suxiao Jiuxin pellet low(SXL) ,medium(SXM) ,high(SXH) dosage group and Astorvastain group(ATO) . Twelve weeks later,the pathological change of Aortas was analyzed by Image Pro Plus system;SDF-1 and CXCR4 were examined by immunohistochemistry. [Results] Compared with Mo,the SXM,SXH and ATO could significantly reduce the arterial intima and media thickness,SMH could also inhibit the proliferation of the collagen fiber and decrease percentage in vessel wall;SXL,SXH,SXN and ATO could decrease the expression of SDF-1 and CXCR4;Between ATO,SXM and SXH there were no significant difference(P0.05) . [Conclusion] Suxiao Jiuxin Pellet(medium,high dosage) can prevent the proceeding of AS by reducing the arterial thickness,inhibiting proliferation of the collagen fiber,delaying the process of AS.
Abstract Objectives Increasing evidences demonstrate a close correlation between epithelial‐to‐mesenchymal transition (EMT) induction and cancer lipid metabolism. However, the molecular mechanisms have not been clarified. Materials and methods In our study, the relative expression level of PRRX1 was detected, its relationship with free fatty acid (FFA) and PPARG2 was analysed in 85 SACC tissues and 15 salivary glands from the benign salivary tumours. We also compared the FFAs composition and levels in these SACC cells. PPARG2 was detected in PRRX1‐induced FFAs treatment as well as Src and MMP‐9 were detected in FFAs treatment–induced invasion and migration of SACC cells, and ChIP test was performed to identify the target interactions. Results Our data showed that overexpression of PRRX1 induced EMT and facilitated the invasion and migration of SACC cells, and PRRX1 expression was closely associated with high FFAs level and poor prognosis of SACC patients. Furthermore, PRRX1 silence led to the increase of PPARG2 and the reduction of FFAs level and the migration and invasion of SACC cells. And inhibition of PPARG2 rescued FFAs level and migration and invasion capabilities of SACC cells. Free fatty acids treatment induced an increase of Stat5‐DNA binding activity via Src‐ and MMP‐9‐dependent pathway . Conclusions Collectively, our findings showed that the PRRX1/PPARG2/FFAs signalling in SACC was important for accelerating tumour metastasis through the induction of EMT and the metabolic reprogramming of FFAs.
Immune-mediated dormancy is that the immune system keeps proliferating tumor cells unchanged mostly via cytotoxic activity of immune cells. Cancer dormancy, especially immune-mediated dormancy, may be the explanation for tumor refractory and be responsible for resistance to conventional chemo- and radiotherapies. Here, we will describe different scenarios of how the immune cells and cytokines involved in cancer progression are connected with the initiation of dormancy and cancer treatment. Two distinct treatments such as maintaining metastatic tumor cells dormant and awakening them are also discussed. A better understanding of immune-mediated dormancy would help to design novel and effective immunotherapies and likely to increase the efficiency of tumor treatment inhibiting metastasis.
Abstract The enhancer of zeste homolog 2 (EZH2), known as a member of the polycomb group (PcG) proteins, is an oncogene overexpressed in a variety of human cancers. Here, we found that EZH2 correlated with poor survival of oral squamous cell carcinoma (OSCC) patients using immunohistochemistry staining. EZH2 overexpression led to a significant induction in tumour glycolysis, Epithelial‐mesenchymal transition (EMT), migration and invasion of OSCC cells. Conversely, silencing of EZH2 inhibited tumour glycolysis, EMT, migration and invasion in OSCC cells. Ectopic overexpression of EZH2 increased phosphorylation of STAT3 at pY705 and decreased FoxO1 expression, and FoxO1 expression was enhanced when inhibiting STAT3. In addition, EZH2 overexpression led to a significant decrease in FoxO1 mRNA levels in nude mice xenograft. These results indicated that regulation of EZH2 might have the potential to be targeted for OSCC treatment.
Immunocompromised and immunocompetent mouse models for head and neck squamous cell carcinoma Zhen-ge Lei,1,* Xiao-hua Ren,2,* Sha-sha Wang,3 Xin-hua Liang,3,4 Ya-ling Tang3,5 1Department of Oral and Maxillofacial Surgery, Stomatological Hospital Affiliated to Nanchang University, Nanchang, Jiangxi, 2Department of Stomatology, Sichuan Medical Science Academy and Sichuan Provincial People's Hospital, 3State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, 4Department of Oral and Maxillofacial Surgery, West China College of Stomatology, Sichuan University, 5Department of Oral Pathology, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, People's Republic of China *These authors contributed equally to this work Abstract: Mouse models can closely mimic human oral squamous epithelial carcinogenesis, greatly expand the in vivo research possibilities, and play a critical role in the development of diagnosis, monitoring, and treatment of head and neck squamous cell carcinoma. With the development of the recent research on the contribution of immunity/inflammation to cancer initiation and progression, mouse models have been divided into two categories, namely, immunocompromised and immunocompetent mouse models. And thus, this paper will review these two kinds of models applied in head and neck squamous cell carcinoma to provide a platform to understand the complicated histological, molecular, and genetic changes of oral squamous epithelial tumorigenesis. Keywords: head and neck squamous cell carcinoma, HNSCC, mouse models, immunocompromised models, immunocompetent models, transgenic models
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