【Abstract】ObjectiveTo investigate the relationship between tumor suppressor gene DPC4 and the development and prognosis of pancreatic carcinoma. MethodsRelevant literatures of recent years were reviewed. ResultsDPC4 was located on chromosome 18. Its product was Smad 4 protein. Smad 4 protein was the central component of the transforming growth factor-beta signaling pathway, and all the biological effect was the results of interaction of Smad 4 and different Smads. The gene was deleted or inactive in about 50% of pancreatic carcinomas. The deletion of DPC4 had a great relation to the development and prognosis of pancreatic carcinoma. ConclusionThe alteration of tumor suppressor gene DPC4 is connected with the development and prognosis of pancreatic carcinoma. However, this research should be further studied.
Objective To investigate the effect of tumor suppressor gene on tumourigenesis in multiple primary malignant neoplasm (MPMN).Methods The retrospective analysis was used to summarize several common tumor suppressor genes correlation to MPMN. Results At current study of the tumor suppressor genes, the common genes studied in MPMN were p53, APC, p16, BRCA1, BRCA2 and PTEN/MMAC1, etc. The same mutation of tumor suppressor genes could be detected from PMNNs. Conclusion There are significant relations between MPMN and inactivation of tumor suppressor gene. By the study of tumor suppressor gene, it can reveal some common rules of tumourigenesis of MPMN.
At present, there are relatively many clinical gene studies. microRNA -215 (miR-215) is a miRNA induced by p53. It exists in animals and humans. miR-215 can exist not only in tumor tissues, but also in blood, urine and feces. miR-215 is abnormally expressed in a variety of tumors and plays a role in promoting and inhibiting cancer. Therefore, miR-215 may provide a new research direction for tumor diagnosis, treatment and prognosis. This paper reviews the expression of miR-215 as a oncogene and tumor suppressor gene in tumors and in non tumors.
ObjectiveTo summarize the role of survivin gene in tumor. MethodsThe research status on biological characteristics the role of survivin gene in tumor for gene therapy and clinical application was retrospectively analyzed after related domestic and foreign literatures were reviewed. ResultsSurvivin gene was by far found to be the best powerful apoptosis inhibition gene, which played antiapoptosis role mainly through inhibiting directly the activity of caspase-3 and caspase-7 in the downstream of cascade reaction. Survivin gene promoted tumor cell proliferation and differentiation through speeding up tumor cells transition of G1→S phase and eluding the recognition of tumor cells to the apoptosis in G2/M phase. Survivin gene played important role in the intermediate links of vasiformation through angiogenic factor (VEGF, bFGF, Ang-1, and COX-2). ConclusionSurvivin gene may inhibit the apoptosis, promote the proliferation and differentiation of tumor cells and tumor angiogenesis, suggested that survivin gene has potential to act as a novel tumor marker and become an indicator of malignant tumor.
【摘要】 目的 探討丙型肝炎病毒非結構蛋白NS4B對肝細胞內p53表達的影響，以及在肝癌發生中的作用與機制。 方法 設置空白對照組、空白載體組、轉染NS4B組、轉染p53組、共轉染NS4B及p53組。使用脂質體介導轉染法，轉染丙型肝炎病毒非結構蛋白重組質粒PCXN2-NS4B及突變型p53基因重組質粒pC53-CX22AN3進入Chang肝細胞內，并用G418篩選獲得穩定表達細胞。采用免疫細胞化學法檢測p53表達率。 結果 空白對照組無p53表達，空白載體組及轉染NS4B組呈弱陽性表達，轉染p53組及共轉染組呈陽性表達；轉染p53組、共轉染組分別與空白對照組、空白載體組及轉染NS4B組比較，差異均有統計學意義 （Plt;0.05）。 結論 NS4B可能抑制p53表達，也可能阻止其進入細胞核，但NS4B與突變型p53關系不明確。NS4B導致肝細胞異常增生，誘導肝癌發生可能不依賴p53的異常表達及突變。【Abstract】 Objective To investigate the effect of hepatitis C Virus on-structural protein 4B(HCV NS4B) on expression of p53 in hepatic cell, and to study the role and mechanism in development of hepatocellular carcinoma. Methods The experiment was divided into negative control, pure vector PCXN2, PCXN2-NS4B, PC53-cx22AN3, and co-transfection group. Recombinant plasmid PCXN2-NS4B and mutant p53 gene--PC53-cx22AN3, PC53-cx22AN3 with PCXN2-NS4B, blank vectors were transfected into Chang liver cell by liposome-mediated transfection respectively. Positive cells were screened by G418. The expression rate of p53 was measured by immunocytochemistry. Result No expression rate of p53 gene in control group was found, lower positive expression in group PCXN2 and PCXN2-NS4B. The expression of p53 gene in group PC53-CX22AN3 and co-transfection was ber than the others (Plt;0.005). Conclusion HCV-NS4B may inhibit the expression of p53 gene, and it may play a crucial role in inhibiting p53 transfered to hepatic cells nuclear. But it isn’t clear that the. HCV-NS4B can enhance the role of mutant p53 gene. It suggested that HCV-NS4B induce proliferation of hepatic cell not through regulating the expression of p53.
Objective To explore the expressions of caudal-related homeodomain transcription factor-2 （CDX-2）and tumor suppressor gene KAI-1 in colon carcinoma tissues and to analyze their clinical significances. Methods Immu-nohistochemical SP method was used to detect the expressions of CDX-2 and KAI-1 in 50 cases of colon carcinoma tissues and corresponding adjacent tissues （from cancer tissue ≤2cm） and 25 cases of normal colon mucosa tissues. The relation-ships of the expressions of CDX-2 and KAI-1 to the clinicopathologic features were analyzed. Results ①The positive rates of CDX-2 expression and KAI-1 expression in the colon carcinoma tissues were significantly lower than those in the normal colon mucosa tissues 〔CDX-2：34% （17/50） versus 88% （22/25）， P＜0.05；KAI-1：30% （15/50） versus 92% （23/25）， P＜0.05〕 and adjacent tissues of colon carcinoma 〔CDX-2：34% （17/50） versus 54% （27/50）， P＜0.05；KAI-1：30% （15/50） versus 58% （29/50）， P＜0.05〕， which in the adjacent tissues of colon carcinoma were significantly lower than those in the normal colon mucosa tissues （P＜0.05）. ②The positive expressions of CDX-2 and KAI-1 were related to lymph node metastasis， depth of invasion， and degree of tumor differentiation （P＜0.05）. ③Spearman rank correl-ation analysis showed that the CDX-2 expression was positively correlated with KAI-1 expression （rs=0.544， P＜0.01）. Conclusions CDX-2 and KAI-1 may be closely related to the development， invasion， metastasis， and prognosis of colon carcinoma， the combination of CDX-2 and KAI-1 in evaluation of their function has a certain guiding significance in the treatment for colon carcinoma.
ObjectiveTo summarize and analyze the relevant studies about the tumor suppressor phosphatase and tensin homolog deleted on chromosome ten (PTEN) and thyroid tumor then further elucidate?the possible mechanism of thyroid tumor formation and progression. Mothods Domestic and international literatures investigating the correlation between PTEN and thyroid tumor were retrieved and reviewed.
ResultsThe abnormal expression of PTEN protein resulted by the mutation or methylation of PTEN gene may up-regulate the expression of its downstream effectors such as PI3K, mTOR, FAK, etc. This probably correlate with thyroid neoplasia and progression. Conciusions Abnormalites of PTEN and its downstream signal ways may correlate with the initiation and development of thyroid tumors. However, the specific mechanism still remains unclear and need more further researches
ObjectiveTo summarize research progress of farnesoid X receptor (FXR) in regulation of hepatocellular carcinoma (HCC) and explore its potential clinical application value.MethodThe relevant literatures at home and abroad on the mechanism of FXR regulating occurrence and development of HCC were reviewed.ResultsIn the occurrence and development of HCC, the FXR expression could be down-regulated through the inflammation-related pathways and epigenetic silencing. The FXR mightbe play an important role in the regulatory mechanisms of down-regulation in the HCC, therapeutic targets, drug resistance, and so on.ConclusionFXR plays an important regulatory role in occurrence and development of HCC, which makes FXR might become a potential target in treatment of HCC.
