| IntroductionHelicobacter pylori (H. pylori) are the causative agent of chronic gastritis and peptic ulcer disease. In the recent years, H. pylori are recognized as an important risk factor for gastric cancer. In China, the incidence of the gastric cancer is higher than that in western countries, and the prevalence of infection with H. pylori is higher too(21 - 93% ). H. pylori infection has become an important public health problem.PC - SPES elicits a multitude of biological responses contributing to its anti - tumor activities. These include disruption of Cell Cycle control and decreased expression of proliferating Cellular nuclear antigen ( PCNA ) , induction of apop-tosis concomitant with down regulation of bcl - 2, and diminution of prostate specific gene expression, exemplified by reduction in the androgen receptor (AR) and PSA levels. The ability of PC - SPES to suppress cancer cell growth is particularly noteworthy and may Principle. However, how PC - SPES induces Cell Cycle arrest is not clear. In this study, We assessed the control of key cell cycle regulatory proteins by PC - SPES. Since PC - SPES blocked G1/S progression in LNCaP cells,we focused on cyclins D and E and Rb. As accomplementary approach, we also used human cell cycles specific cDNA array to characterize the transcriptional responses of LNCaP cancer cells to PC - SPES and to establish a method that Will permit identification of genes with Obligatory or facilitory roles in the PC - SPES mediated cell cycle control. To determine the association between Helicobacter pylori (Hp) and the gastric cancer by Meta - analysis. The paper collected 36 papers about the association between Hp infection and thegastric cancer. The method introduced by Fleiss was used to calculate the OR and 95% CI and Meta - analysis was applied to determine the association between HP infection and gastric cancer.Subjects and MethodsRelative changes in cell cycle regulatory protein expression in control and PC - SPES treated LNCaP cells. Expression of cyclin D and E in 3 ul/ml day 1 - 3 PC - SPES treated cells was assessed by immunoblot analysis. The intensities of the cyclin D and E bands were quantitated by densitometry and presented as % suppression against control. Expression of actin was used as an internal control to verify equivalent protein loading. Results were averaged from 3 independent experiment and presented as means SD. The paper collected 36 papers about the association between Hp infection and the gastric cancer. The method introduced by Fleiss was used to calculate the OR and 95% CI and Meta - analysis was applied to determine the association between HP infection and gastric cancer.ResultsPC - SPES is an herbal mixture, with evidence of clinical efficacy against cancer (CAP), recently attracting tremendous attention. Using immunoblot and cell cycle specific cDNA array analyses, PC - SPES inhibited expression of cyc-lins D and E, inhibited Rb phosphorylation, switching it to a Gl - to - S inhibitory state. Moreover, cDNA array analysis showed that PC - SPES caused up -regulation of p21 and decreased expression of cyclin B, Nedd8, cdc2,skpl, PCNA, MAD2L1, cyclin H, CKS2, E2F, Rbxl, MCM2, MCM5, Mpp2, Cullin - Cul4A, Ckslp9 and McMT, which are involved in cell cycle progression. There were 4238 gastric cancer cases in which there were 3385(79. 88%) people with Hp positive and 6435 controls in which 3890(60. 82%) people with Hp positive. The incorporated OR was 2. 37(95% CI: 2. 14 -2. 61, x2 = 171. 14, P < 0. 01) by the Meta - analysis. The early vs. developing stage of thecancer, OR = 2. 25 (95% CI: 1. 36 - 3. 74) ; Non - cardiac gastric cancer vs. cardiac gastric cancer, OR = 2. 57(95% CI: 1.78-3.27) ;Intestinal metaplasia gastric cancer vs. diffusion gastric cancer, OR = 1. 11 (95% CI: 0.87-1. 42) ; male vs. female, OR = 1. 05 (95% CI: 0. 75 - 1. 47) ; The controls in hospitals vs. controls in population, OR = 0.92 (95% CI = 0.78 - 1. 08 ).DiscussionThe mortality of gastric carcinoma has been ranked the first in the leading of death in our country. Study on the occurrence and developing mechanism of gastric cancer and exploring reasonable and effective prevention methods will be very important for early prevention of gastric cancer and reducing the recurrence after operation. Epidemiology studies show that there is significant relationship between Helicobacter pylori (Hp) infection and development of gastric cancer. As many other tumors, gastric cancer developing depends on not single factor but many factors. Those factors are involved in various stages of gastric cancer developing. It is now regarded that gastric cancer may be possible the results of the interaction between constant Hp infection and many other factors. Hp infection may be the first step factor. It is found that Hp acts at the initiation stage of the forming process of gastric cancer and Hp is considered an initial factor of gastric development. Recent studies showed that Hp infection might cause abnormality of proliferation and apoptosis of gastric mucous epithelial cells and disequilibrium between them play an important role in the development of gastric cancer. In the forming process of gastric cancer, there is not only cell proliferation but also cell apoptosis. But in the tumor cells there are ratio imbalance. When cells traverse the G0 to G1 phase to S - phase transition, a series of cyclin - dependent kinases is activated. The addition of serum growth factors to quiescent cells promotes transcription of the cyclin D gene. Cyclin D then associates with pre - existing cdk4 to form an active complex. The kinase activity associated with this complex can phosphorylate specific sites on the retinoblastoma protein ( pRb), leading to inactivation of pRb and the activation cyclin E transcription by E2F. Activation of the cyclin E gene can be blocked by the cdk inhibitor... |
