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Insulin, longevity, and genetic analysis of metabolism

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Protein & Cell 2010年第7期1卷 605-606页

作者： steven y cheng Department of Developmental Genetics center for Regenerative Medicine Nanjing Medical UniversityNanjing 210029China

In a 1989 Hollywood hit“Sex,Lies,and Videotapes”,director steven Soderbergh told a story of an incestuous affair between a hot-shot lawyer and the sister of his married *** over-stayed visit by a drifter whose unusual fetish of videotaping conversations about sex lives of women deconvoluted this adulterous *** the biological life,persistent bias can also throw off a balance such as the homeostasis delicately constructed among metabolism,longevity,and the insulin signaling *** a recent paper published in Cell Metabolism,yong Liu’s group at the Shanghai Institute of Nutritional Sciences and Liangyou Rui’s group at the University of Michigan Medical School reported that alteration of metabolism through genetic deletion of SH2B,a gene encoding an adaptor protein required for insulin signaling,causes significant changes in the life span of affected fruitflies and *** the manmade and the god-made stories show only a slight superficial analogy in form,they both unfold through serendipitous analyses of seemingly unrelated events,a theme that reoccurringly underscores the importance of basic research.

关键词： metabolism analogy conversation

Complete reprogramming to all-iPS mice

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Protein & Cell 2010年第1期1卷 2-3页

作者： steven y cheng Department of Developmental Genetics and Center for Regenerative Medicine Nanjing Medical UniversityNanjing 210029China

The landmark discoveries by Shinya yamanaka in mice and later separately by James Thompson in humans that adult animal cells can be reprogrammed to a pluripotent state of embryonic stem(ES)cells by forced expression of just a few key transcription factors have permanently altered a long-held view about the stability of differentiated cells in developmental biology,and suggested a way of generating personalized replacement tissues from patients’own cells for the regenerative medical treatment.

关键词： programming generating permanent

Smurfs have“fused”into the asymmetric division of stem cells

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Protein & Cell 2011年第1期2卷 2-4页

作者： steven y.cheng ying E.Zhang Department of Developmental Genetics Center for Regenerative MedicineNanjing Medical University140 Hanzhong RoadNanjing 210029China Laboratory of Cellular and Molecular Biology National Cancer InstituteNational Institutes of Health37 Convent DriveBethesdaMD 20892USA

The asymmetric cell division is the way in which a stem cell divides into one daughter stem cell and one differentiated daughter *** process is one of the key principles of developmental biology that ensures the perpetual supply of stem cells while allowing a particular cell lineage to be *** Drosophila oogenesis,the fate of the daughter stem cell produced from the asymmetric division of germline stem cells(GSCs)is specified by Decapentaplegic(Dpp),but the other daughter cell has almost equal access to the Dpp *** Dpp signaling is inactivated in the differentiated daughter cell has been a deep mystery until a recent study,led by Dahua Chen of the Institute of Zoology,China(Xia et al.,2010),showed that the Dpp receptor,Thick vein(Tkv),is degraded specifically in the differentiated daughter cell by an HECT-domain ubiquitin E3 ligase,Smurf,in conjunction with a serine-threonine kinase Fused(Fu).This finding is as much revealing as it is surprising,because up until now Fu is considered a core member of the Hedgehog signaling pathway.

关键词： daughter asymmetric fused

Identification of four novel prognosis biomarkers and potential therapeutic drugs for human colorectal cancer by bioinformatics analysis

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The Journal of Biomedical Research 2021年第1期35卷 21-35,I0005-I0013页

作者： Zhen Sun Chen Liu steven y.cheng Department of Medical Genetics 2Department of Pathology and Pathophysiology3Jiangsu Key Lab of Cancer BiomarkersPrevention and TreatmentCollaborative Innovation Center for Cancer Personalized MedicineNanjing Medical UniversityNanjingJiangsu 211166China.

Colorectal cancer(CRC)is one of the most deadly cancers in the world with few reliable biomarkers that have been selected into clinical guidelines for prognosis of CRC *** this study,mRNA microarray datasets GSE113513,GSE21510,GSE44076,and GSE32323 were obtained from the Gene Expression Omnibus(GEO)and analyzed with bioinformatics to identify hub genes in CRC *** expressed genes(DEGs)were analyzed using the GEO2 R *** ontology(GO)and KEGG analyses were performed through the DAVID *** database and Cytoscape software were used to construct a protein-protein interaction(PPI)network and identify key modules and hub *** analyses of the DEGs were performed on GEPIA *** Connectivity Map database was used to screen potential drugs.A total of 865 DEGs were identified,including 374 upregulated and 491 downregulated *** DEGs were mainly associated with metabolic pathways,pathways in cancer,cell cycle and so *** PPI network was identified with 863 nodes and 5817 *** analysis revealed that HMMR,PAICS,ETFDH,and SCG2 were significantly associated with overall survival of CRC *** blebbistatin and sulconazole were identified as candidate *** conclusion,our study found four hub genes involved in CRC,which may provide novel potential biomarkers for CRC prognosis,and two potential candidate drugs for CRC.

关键词： colorectal cancer Gene Expression Omnibus biomarkers bioinformatics analysis

The role of microRNAs during the genesis of medulloblastomas induced by the hedgehog pathway

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The Journal of Biomedical Research 2011年第1期25卷 42-48页

作者： steven y cheng Department of Developmental Genetics and Center for Regenerative Medicine Nanjing Medical University

Constitutive hedgehog （Hh） signaling is associated with the genesis of medulloblastomas （MB）. The objective of this study is to identify special microRNAs （miRNAs） regulated by the Hh pathway, and to clarify the role of miRNAs during the genesis of MB induced by sustained Hh activation. In the primary screening, we used stemloop RT-PCR to test the expression of 90 different miRNAs in the wildtype （WT） and Ptc-/- MEF cell lines. In the secondary screening, the miRNAs screened from the first screening were validated in the Sufu-/- MEF cell lines. We then verified the expression of miRNAs both in the normal cerebellar tissues and the MB induced by activated Hh pathway, and examined the expression of the other 21 miRNA members of the miR-154 cluster in the MB and normal cerebellum. In the first screening, 13 miRNAs showed significant differential expression in WT and Ptc-/- MEF cell lines, while 10 of them had significant difference in the Sufu-/- MEF cell line. Compared to the normal mouse cerebellum, only 2 miRNAs in 15 miRNAs were differentially expressed between the MB and normal cerebellar tissues. Among 21 members of the miR-154 cluster, 6 miRNAs were downregulated in the MB. Our study demonstrated that miR-154 may be regulated by the Hh pathway, and the activation of the Hh pathway led to the downregulation of the miR-154 cluster, resulting in the genesis of MB.

关键词： Hedgehog signaling pathway microRNAs miR-154 cluster medulloblastomas

Sonic Hedgehog stimulates migration of MCF-7 breast cancer cells through Rac1

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The Journal of Biomedical Research 2019年第5期33卷 297-307页

作者： Tian Shen Bo'ang Han yan Leng Sen yan Junfeng Shi Shen yue steven y cheng Jiangsu Key Laboratory o f Xenotransplanation Department of Medical GeneticsCollaborative Innovation Center for Cancer Personalized MedicineNanjing Medical UniversityNanjingJiangsu 211166China Department of Pathology andPathophysiology Collaborative Innovation Center for Cancer Personalized MedicineNanjing Medical UniversityNanjingJiangsu 211166China Jiangsu Key Lab of Cancer Biomarkers Prevention and TreatmentCollaborative Innovation Center for Cancer Personalized MedicineNanjing Medical UniversityNanjingJiangsu 211166China Department of Pathology Jiangsu Province HospitalNanjingJiangsu 210029China Department of Oncology Nanjing First Hospital Affiliated to Nanjing Medical UniversityNanjingJiangsu 210006China.

As one of the most common tumors in women, breast cancer has drawn considerable interest from investigators and clinicians in recent years. Despite early diagnosis and best therapeutic regimens available, the prognosis of malignant or metastatic breast cancer patients is still not optimistic. Hedgehog signaling, a classical pathway indispensable to embryonic development, participates in the growth of a variety of tumors. In the present study,the effect of Sonic Hedgehog(Shh) on breast cancer cells was investigated. We identified that Shh signal stimulated the migration of MCF-7 breast cancer cells. Smo and Gli1 were involved in Shh-stimulated migration of MCF-7 cells. Activating Smo and Gli1 induced cell migration, which was blocked by their specific *** effect of Shh signaling on MCF-7 cells was independent of Wnt5 a, Dvl2 and Rab35, but directly dependent on Rac1. In conclusion, our study suggested that Shh promotes breast cancer cell migration via Rac1 independently of the non-canonical Wnt signaling pathway, which may represent a rational molecular target for combination medication in breast cancer.

关键词： Sonic Hedgehog Rac1 breast cancer MCF-7 migration

Hedgehog signaling regulates phosphorylation and ubiquitination of Suppressor of fused

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Hedgehog signaling regulates phosphorylation and ubiquitinat...

Understanding Hedgehog signaling in development and cancer

“细胞活动生命活力”——中国细胞生物学学会全体会员代表大会暨第十二次学术大会

作者： steven y cheng Department of Developmental Genetics and Center for Regenerative Medicine Nanjing Medical UniversityNanjingJiangsu 210029China

Suppressor of fused(Sufu) is an essential negative regulator in the sonic hedgehog(Shh) pathway,but it is not clear how its inhibition of Shh signaling is alleviated to allow for the activation of downstream targets. To address this issue,we examined the turnover of Sufu mediated by the ubiquitin-proteasome system,and found that Shh signaling promotes the ubiquitination of *** with this result,the level of total Sufu was found to be decreased significantly in Ptch null MEFs,in which Shh signaling is inappropriately *** analysis by mass spectrometry,we determined that the ubiquitin modification of Sufu occurs on K257,which is likely to be a key residue affecting Sufu stability as the K257R mutant of Sufu was more stable and potent as a repressor of the Gli1 transcriptional activity as well as cell growth when tested in NCI-H322M lung cancer *** further found that cAMP-dependent protein kinase A(PKA), another important negative regulator in the Shh pathway,has a strong stabilizing effect on Sufu when Sufu was co-expressed with the catalytic subunit of *** again,we identified two serine residues,S342 and S346,as the sites of PKA-mediated phosphorylation by mass spectrometry,and showed that the S342/346A double mutant of Sufu is much less stable than its wild type counterpart.S346 is a consensus GSK3 recognition site whereas S342 is a typical PKA *** data showed that phosphorylation at S342 by PKA likely follows a priming event at S346 by GSK3;it is also likely to occur in vivo as evident by the detection with a poly-clonal antibody that is capable of recognizing the endogenous S342-phosphorylated form of ***,the levels of S342-phosphorylated form of as well as the total Sufu were found to be increased significantly in Smo null MEFs,which is a reciprocal corroboration to the results obtained from Ptch null *** together,these data suggest that Shh signaling likely promotes Sufu degradation through the ubiquitin

关键词： Sufu Shh phosphorylation ubiquitination

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Understanding Hedgehog signaling in development and cancer

The miR-183～96～182 cluster promotes tumorigenesis in a mouse model of medulloblastoma

2012全国发育生物学大会

作者： steven y.cheng Department of Developmental Genetics School of Basic Medical SciencesNanjing Medical University

Hedgehog is a majordevelopmental signal that specifies cell fate and tissue shape during morphogenesis of many tissues,including the *** Hedgehog signal goes awry,cancer ensues;suchis the case in the cerebellar tumor *** recently showed that loss of a single allele of tumor suppressor gene Pten can drastically accelerate the spontaneous onset of medulloblastoma in the Hedgehog receptor Patched(Ptch) mutant mouse model(Ptch-/+), suggesting that the Akt-Pten and Hedgehog pathways cooperatively safe-guard developing cerebellar granular neuron precursors from undergoing oncogenic *** intersecting nodes between these two pathways will be discussed.A hallmark of the Hedgehog signaling system is the ability of receiving cells to perceive and respond accordingly to the morphogenic instructions encoded in the Hedgehog signal *** the level of cell surface,Hedgehog controls the trafficking of a pair of counter-acting membrane receptors,Ptch and Smoothened,into the primary cilium,a cell surface protruding organelle akin to a signaling *** the nucleus,transcription of vertebrate Hedgehog target genes is controlled by another gradient of positive and negative transcription factors,formed by a mixture of full length Gli1,2,and 3 activators and their proteolyticaily processed and truncated inhibitory variants.I will report our recent identification of an enzymatic system that controls the ciliary movement of Ptch and our long term investigation of the role of Suppressor of fused in regulating Gli transcriptional activities.

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The Journal of Biomedical Research 2013年第6期27卷 486-494页

作者： Zengdi Zhang Sanen Li steven y cheng Department of Developmental Genetics Nanjing Medical University

Medulloblastoma is the most common malignant pediatric brain tumor. Some are thought to originate from cerebellar granule neuron progenitors （CGNPs） that fail to undergo normal cell cycle exit and differentiation. The contribution of microRNAs to the initiation and progression of medulloblastoma remains poorly understood. Increased expression of the miR-183-96-182 cluster of microRNAs has been noted in several aggressive sub- groups. We identified that expression of miR-183-96-182 was higher in medulloblastomas with Pten gene loss in the background of the activated sonic hedgehog （Shh） signaling pathway. Ectopic miR-183-96-182 expression in CGNPs synergized with exogenous Shh to increase proliferation and its role depended on hedgehog signaling ac- tivation. Our findings suggest a new microRNA cluster, the miR-183-96-182, functionally collaborates with the Shh signaling pathway in the development of medulloblastomas in mice.

关键词： medulloblastoma microRNAs Shh pathway granule neuron progenitors proliferation