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Association of RNF43 with cell cycle proteins involved in p53 pathway.

ABSTRACT: Our previous study has demonstrated that RNF43 could regulate the cell cycle in a p53-dependent manner in HCC. In this study, we aimed to access whether RNF43 could interact with cell cycle proteins involved in p53 pathway, including pRB, Cyclin D1 and MDM2. Totally, 123 paired HCC tissues and corresponding noncancerous tissues from HCC patients were included, and the expression of Cyclin D1, pRB and MDM2 was analyzed using tissue microarray. Our results showed the expression level of RNF43 in HCC was positively correlated with that of MDM2, Cyclin D1 and pRB-S780. There was no significant correlation between the expression of RNF43 and pRB-S807/S811. Indicating that RNF43 effected cell cycling by regulating the expression of pRB, Cyclin D1 and MDM2 proteins, and pRB-S780 but not pRB-S807/S811, was participated in RNF43 regulated cell cycling.

SUBMITTER: Xie H

PROVIDER: S-EPMC4713620 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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Association of RNF43 with cell cycle proteins involved in p53 pathway.

Xie Haiyang H Xing Chunyang C Cao Guoqiang G Wei Bajin B Xu Xiao X Song Penghong P Chen Leiming L Chen Hai H Yin Shengyong S Zhou Lin L Zheng Shusen S

International journal of clinical and experimental pathology 20151101 11

Our previous study has demonstrated that RNF43 could regulate the cell cycle in a p53-dependent manner in HCC. In this study, we aimed to access whether RNF43 could interact with cell cycle proteins involved in p53 pathway, including pRB, Cyclin D1 and MDM2. Totally, 123 paired HCC tissues and corresponding noncancerous tissues from HCC patients were included, and the expression of Cyclin D1, pRB and MDM2 was analyzed using tissue microarray. Our results showed the expression level of RNF43 in H ...[more]

PMID: 26823834

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Project description:ObjectivesCancer cells differ from normal body cells in their ability to divide indefinitely and to evade programmed cell death. Crosstalk between apoptosis and cell cycle processes promotes balance between proliferation and death, and limits population growth and survival of cells. However, intricate relationships between them and how they are able to manipulate the fate of cancer cells still remain to be clarified. Identification of key factors involved in both apoptosis and cell cycle regulation may help to address this problem.Materials and methodsIdentification of such key proteins was carried out, using a series of bioinformatics methods, such as network construction and key protein identification.ResultsIn this study, we computationally constructed human apoptotic/cell cycle-related protein-protein interactions (PPIs) networks from five experimentally supported protein interaction databases, and further integrated these high-throughput data sets into a Naïve Bayesian model to predict protein functional connections. On the basis of modified apoptotic/cell cycle related PPI networks, we calculated and ranked all protein members involved in apoptosis and cell cycle regulation. Our results not only identified some already known key proteins such as p53, Rb, Myc and Src but also found that the proteasome, Cullin family members, kinases and transcriptional repressors play important roles in regulating apoptosis and the cell cycle. Furthermore, we found that the top 100 proteins ranked by PeC were enriched in some pathways such as those of cancer, the proteasome, the cell cycle and Wnt signalling.ConclusionsWe constructed the global human apoptotic/cell cycle related PPI network based on five online databases, and a Naïve Bayesian model. In addition, we systematically identified apoptotic/cell cycle related key proteins in cancer cells. These findings may uncover intricate relationships between apoptosis and cell cycle processes and thus provide further new clues towards future anticancer drug discovery.

Project description:BackgroundDespite the advancement in chemotherapeutic drugs for colon cancer treatment, it is still a life-threatening disease worldwide due to drug resistance. Therefore, an urgently needed to develop novel drugs for colon cancer therapies. AGA is a combination of traditional Chinese medicine Antler's extract (A), Ganoderma lucidum (G), and Antrodia camphorata (A); it contains a lot of biomolecules like polysaccharides, fatty acids, and triterpenoids that are known to exerting anti-oxidative, anti-inflammatory, anti-microbial and anti-tumor activities in oral cancer. In this study, we investigate AGA anti-proliferative, anti-metastatic and apoptotic activity to explore its anti-cancer activity against colon cancer cells and its underlying mechanism.MethodHere, in-vitro studies were performed to determine the antiproliferative activity of AGA through MTT and colony formation assays. Wound healing and transwell migration assay were used to evaluate the metastasis. Flow cytometry and protein expression were used to investigate the involved molecular mechanism by evaluating the cell cycle and apoptosis. The in-vivo anti-cancerous activity of AGA was assessed by xenograft mice model of colon cancer cells.ResultsWe found that AGA significantly inhibited the proliferative capacity and metastasis of colon cancer cells in-vitro. In addition, AGA induced cell cycle arrest in the sub-G1 phase through upregulating p21 and downregulating CDK2, CDK6 in SW620, and CDK4 in SW480 and HT29, respectively. Annexin-v assay indicated that colon cancer cells had entered early and late apoptosis after treatment with AGA. Furthermore, a mechanistic protein expressions study revealed that AGA in p53-dependent and independent regulated the apoptosis of colon cancer by downregulating the p53 protein expression in SW620 and SW480 cells but upregulating in a dose-dependent manner in HT29 cells and increasing the expression of Bax and caspase-9 to inhibit the colon cancer cells. In vivo study, we found that AGA significantly reduced the xenograft tumor growth in NOD/SCID mice with no adverse effect on the kidney and liver.ConclusionCollectively, AGA has the potential to inhibit colon cancer through inhibiting proliferation, migration, and cell cycle kinase by upregulating p21 protein expression and promoting the apoptotic protein in a p53-dependent and independent manner.

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Association of RNF43 with cell cycle proteins involved in p53 pathway.

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Association of RNF43 with cell cycle proteins involved in p53 pathway.

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