Death inducer-obliterator 1 (Dido1) is a BMP target gene and promotes BMP-induced melanoma progression.

Abstract:

:Bone morphogenetic proteins (BMPs) are known to play an important role in melanoma development and progression. However, the downstream targets of BMPs have not been investigated thus far. Therefore, we treated melanoma cell lines with the Smad-specific BMP inhibitor Dorsomorphin and performed a cDNA microarray. We identified death inducer-obliterator 1 (Dido1) as a BMP-specific Smad-regulated target gene, which was confirmed by qRT-PCR, immunofluorescence staining and electrophoretic mobility shift assay experiments. An analysis of Dido1 expression revealed an upregulation of Dido1 levels in melanoma cell lines and tissues compared with normal melanocytes. Colony-formation assays showed that siDido1-transfected cells formed significantly smaller colonies when grown in soft agar compared with control cells. In addition, fluorescence-activated cell sorting and western blot experiments revealed that transfection of melanoma cells with Dido1 small interfering RNAs led to an upregulation of apoptosis. Furthermore, cell migratory and invasive potentials were strongly reduced in siDido1-transfected cells compared with control cells. Finally, we demonstrated that Dido1 induces the expression of Integrin αV, thereby promoting the attachment, migration, invasion and apoptosis resistance of melanoma cells.

journal_name

Oncogene

journal_title

Oncogene

authors

Braig S,Bosserhoff AK

doi

10.1038/onc.2012.115

subject

Has Abstract

pub_date

2013-02-14 00:00:00

pages

837-48

issue

7

eissn

0950-9232

issn

1476-5594

pii

onc2012115

journal_volume

32

pub_type

杂志文章

相关文献

ONCOGENE文献大全
  • Tip60 degradation by adenovirus relieves transcriptional repression of viral transcriptional activator EIA.

    abstract::Adenoviruses are linear double-stranded DNA viruses that infect human and rodent cell lines, occasionally transform them and cause tumors in animal models. The host cell challenges the virus in multifaceted ways to restrain viral gene expression and DNA replication, and sometimes even eliminates the infected cells by ...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/onc.2012.534

    authors: Gupta A,Jha S,Engel DA,Ornelles DA,Dutta A

    更新日期:2013-10-17 00:00:00

  • Reexpression of epigenetically silenced AML tumor suppressor genes by SUV39H1 inhibition.

    abstract::Reexpression of hypermethylated tumor suppressor genes using DNA methyltransferase (DNMT) and histone deacetylase inhibitors occurs by a mechanism whereby promoter demethylation is the dominant event. In support of this model, we found in acute myeloid leukemia cells with hypermethylated p15INK4B and E-cadherin promot...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/onc.2009.361

    authors: Lakshmikuttyamma A,Scott SA,DeCoteau JF,Geyer CR

    更新日期:2010-01-28 00:00:00

  • Apoptosis and melanoma chemoresistance.

    abstract::Melanoma is the most aggressive form of skin cancer and is notoriously resistant to all current modalities of cancer therapy. A large set of genetic, functional and biochemical studies suggest that melanoma cells become 'bullet proof' against a variety of chemotherapeutic drugs by exploiting their intrinsic resistance...

    journal_title:Oncogene

    pub_type: 杂志文章,评审

    doi:10.1038/sj.onc.1206454

    authors: Soengas MS,Lowe SW

    更新日期:2003-05-19 00:00:00

  • Oncogenic transformation by beta-catenin: deletion analysis and characterization of selected target genes.

    abstract::Genetic analysis of beta-catenin-induced oncogenic transformation in chicken embryo fibroblasts (CEF) revealed the following prerequisites for oncogenicity: (1) removal of the N terminal phosphorylation sites targeted by glycogen synthase kinase 3beta (GSK3beta), (2) retention of the N terminal transactivation domain,...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1205796

    authors: Aoki M,Sobek V,Maslyar DJ,Hecht A,Vogt PK

    更新日期:2002-10-10 00:00:00

  • Isolation of a new class of 'flat' revertants from ras-transformed NIH3T3 cells using cis-4-hydroxy-L-proline.

    abstract::A new class of nontransformed revertant cells has been isolated from the ras-transformed cell line DT using cis-4-hydroxy-L-proline (CHP) as a selective agent. The new revertants, CHP 9CJ and CHP CB4, each contain two copies of the v-Ki-ras gene, elevated levels of phosphorylated p21ras protein, and rescuable transfor...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:

    authors: Yanagihara K,Ciardiello F,Talbot N,McGeady ML,Cooper H,Benade L,Salomon DS,Bassin RH

    更新日期:1990-08-01 00:00:00

  • The p53 gene family.

    abstract::p73 and p63 are two recently discovered p53 homologs. Like p53, these proteins can recognize canonical p53 DNA-binding sites and, when overproduced, can activate p53-responsive target genes and induce apoptosis. Unlike p53, these genes undergo complex alternative splicing which, at least in the case of p63, yields pro...

    journal_title:Oncogene

    pub_type: 杂志文章,评审

    doi:10.1038/sj.onc.1202955

    authors: Kaelin WG Jr

    更新日期:1999-12-13 00:00:00

  • Bone morphogenetic protein 3B silencing in non-small-cell lung cancer.

    abstract::Bone morphogenetic protein 3B (BMP3B) is a member of the TGF-beta superfamily. The BMP3B promoter sequence was previously identified as a target for aberrant DNA methylation in non-small-cell lung cancer (NSCLC). Aberrant DNA hypermethylation in the BMP3B promoter is associated with downregulation of BMP3B transcripti...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1207441

    authors: Dai Z,Popkie AP,Zhu WG,Timmers CD,Raval A,Tannehill-Gregg S,Morrison CD,Auer H,Kratzke RA,Niehans G,Amatschek S,Sommergruber W,Leone GW,Rosol T,Otterson GA,Plass C

    更新日期:2004-04-29 00:00:00

  • The DNA damage signalling kinase ATM is aberrantly reduced or lost in BRCA1/BRCA2-deficient and ER/PR/ERBB2-triple-negative breast cancer.

    abstract::The ataxia-telangiectasia-mutated (ATM) kinase is a key transducer of DNA damage signals within the genome maintenance machinery and a tumour suppressor whose germline mutations predispose to familial breast cancer. ATM signalling is constitutively activated in early stages of diverse types of human malignancies and c...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1210885

    authors: Tommiska J,Bartkova J,Heinonen M,Hautala L,Kilpivaara O,Eerola H,Aittomäki K,Hofstetter B,Lukas J,von Smitten K,Blomqvist C,Ristimäki A,Heikkilä P,Bartek J,Nevanlinna H

    更新日期:2008-04-10 00:00:00

  • Non-canonical activation of hedgehog in prostate cancer cells mediated by the interaction of transcriptionally active androgen receptor proteins with Gli3.

    abstract::Hedgehog (Hh) is an oncogenic signaling pathway that regulates the activity of Gli transcription factors. Canonical Hh is a Smoothened- (Smo-) driven process that alters the post-translational processing of Gli2/Gli3 proteins. Though evidence supports a role for Gli action in prostate cancer (PCa) cell growth and prog...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/s41388-017-0098-7

    authors: Li N,Truong S,Nouri M,Moore J,Al Nakouzi N,Lubik AA,Buttyan R

    更新日期:2018-04-01 00:00:00

  • HNF4alpha reduces proliferation of kidney cells and affects genes deregulated in renal cell carcinoma.

    abstract::Hepatocyte nuclear factor 4alpha (HNF4alpha) is a tissue-specific transcription factor known to regulate a large number of genes in hepatocytes and pancreatic beta cells. Although HNF4alpha is highly expressed in some sections of the kidney, little is known about its role in this organ and about HNF4alpha-regulated ge...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1208794

    authors: Lucas B,Grigo K,Erdmann S,Lausen J,Klein-Hitpass L,Ryffel GU

    更新日期:2005-09-22 00:00:00

  • A novel mitochondrial amidoxime reducing component 2 is a favorable indicator of cancer and suppresses the progression of hepatocellular carcinoma by regulating the expression of p27.

    abstract::Hepatocellular carcinoma (HCC) is the fifth leading cause of cancer-related mortality in the United States. Exploring the mechanism of HCC and identifying ideal targets is critical. In the present study, we demonstrated metabolism dysfunction might be a key diver for the development of HCC. The mitochondrial amidoxime...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/s41388-020-01417-6

    authors: Wu D,Wang Y,Yang G,Zhang S,Liu Y,Zhou S,Guo H,Liang S,Cui Y,Zhang B,Ma K,Zhang C,Liu Y,Sun L,Wang J,Liu L

    更新日期:2020-09-01 00:00:00

  • Overexpression of androgen receptor enhances the binding of the receptor to the chromatin in prostate cancer.

    abstract::Androgen receptor (AR) is overexpressed in the majority of castration-resistant prostate cancers (CRPCs). Our goal was to study the effect of AR overexpression on the chromatin binding of the receptor and to identify AR target genes that may be important in the emergence of CRPC. We have established two sublines of LN...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/onc.2011.401

    authors: Urbanucci A,Sahu B,Seppälä J,Larjo A,Latonen LM,Waltering KK,Tammela TL,Vessella RL,Lähdesmäki H,Jänne OA,Visakorpi T

    更新日期:2012-04-26 00:00:00

  • Mimicking the BH3 domain to kill cancer cells.

    abstract::Cancer cells show deviant behavior that induces apoptotic signaling. To survive, cancer cells typically acquire changes enabling evasion of death signals. One way they do this is by increasing the expression of anti-apoptotic BCL-2 proteins. Anti-apoptotic BCL-2 family proteins antagonize death signaling by forming he...

    journal_title:Oncogene

    pub_type: 杂志文章,评审

    doi:10.1038/onc.2009.52

    authors: Ni Chonghaile T,Letai A

    更新日期:2008-12-01 00:00:00

  • MTHFD2 links RNA methylation to metabolic reprogramming in renal cell carcinoma.

    abstract::One-carbon metabolism plays a central role in a broad array of metabolic processes required for the survival and growth of tumor cells. However, the molecular basis of how one-carbon metabolism may influence RNA methylation and tumorigenesis remains largely unknown. Here we show MTHFD2, a mitochondrial enzyme involved...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/s41388-019-0869-4

    authors: Green NH,Galvan DL,Badal SS,Chang BH,LeBleu VS,Long J,Jonasch E,Danesh FR

    更新日期:2019-08-01 00:00:00

  • Differential induction of c-fos and c-jun proto-oncogenes and AP-1 activity by tumor promoter 12-O-tetradecanoyl phorbol 13-acetate in cells at different stages of tumor promotion in vitro.

    abstract::A two-stage (initiation and promotion) model of chemical transformation of mouse embryonic fibroblasts was used to elucidate the molecular mechanisms of tumor promotion in vitro. C3H10T1/2 cells which had been initiated with a subcarcinogenic dose (0.5 micrograms ml-1) of benzo[a]pyrene (B[a]P) were isolated after 12-...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:

    authors: Wu WS,Lin JK,Wu FY

    更新日期:1992-11-01 00:00:00

  • FKBP51 and Cyp40 are positive regulators of androgen-dependent prostate cancer cell growth and the targets of FK506 and cyclosporin A.

    abstract::Prostate cancer (PCa) growth is dependent on androgens and on the androgen receptor (AR), which acts by modulating gene transcription. Tetratricopeptide repeat (TPR) proteins (FKBP52, FKBP51 and Cyp40) interact with AR in PCa cells, suggesting roles in AR-mediated gene transcription and cell growth. We report here tha...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/onc.2009.458

    authors: Periyasamy S,Hinds T Jr,Shemshedini L,Shou W,Sanchez ER

    更新日期:2010-03-18 00:00:00

  • CNOT3 targets negative cell cycle regulators in non-small cell lung cancer development.

    abstract::Lung cancer is one of the major causes of cancer death and clarification of its molecular pathology is highly prioritized. The physiological importance of mRNA degradation through the CCR4-NOT deadenylase has recently been highlighted. For example, mutation in CNOT3, a gene coding for CNOT3 subunit of the CCR4-NOT com...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/s41388-018-0603-7

    authors: Shirai YT,Mizutani A,Nishijima S,Horie M,Kikuguchi C,Elisseeva O,Yamamoto T

    更新日期:2019-04-01 00:00:00

  • ROS release by PPARβ/δ-null fibroblasts reduces tumor load through epithelial antioxidant response.

    abstract::Tumor stroma has an active role in the initiation, growth, and propagation of many tumor types by secreting growth factors and modulating redox status of the microenvironment. Although PPARβ/δ in fibroblasts was shown to modulate oxidative stress in the wound microenvironment, there has been no evidence of a similar e...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/s41388-017-0109-8

    authors: Tan EHP,Sng MK,How ISB,Chan JSK,Chen J,Tan CK,Wahli W,Tan NS

    更新日期:2018-04-01 00:00:00

  • Regulation of SV40 large T-antigen stability by reversible acetylation.

    abstract::Reversible acetylation on protein lysine residues has been shown to regulate the function of both nuclear proteins such as histones and p53 and cytoplasmic proteins such as alpha-tubulin. To identify novel acetylated proteins, we purified several proteins by the affinity to an anti-acetylated-lysine antibody from cell...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1209731

    authors: Shimazu T,Komatsu Y,Nakayama KI,Fukazawa H,Horinouchi S,Yoshida M

    更新日期:2006-11-30 00:00:00

  • A model for GFR alpha 4 function and a potential modifying role in multiple endocrine neoplasia 2.

    abstract::Mutations of the RET proto-oncogene are found in the majority of patients with the inherited cancer syndrome multiple endocrine neoplasia type 2 (MEN 2). A minority of cases, however, have no detectable RET mutation and there is considerable phenotypic variation within and among MEN 2 families with the same RET mutati...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1207826

    authors: Vanhorne JB,Andrew SD,Harrison KJ,Taylor SA,Thomas B,McDonald TJ,Ainsworth PJ,Mulligan LM

    更新日期:2005-02-03 00:00:00

  • Feline STK gene expression in mammary carcinomas.

    abstract::The human RON and its mouse homologue stk are members of the MET family of tyrosine kinase receptors. We have previously shown that the RON gene is over-expressed in human breast carcinomas. As cat mammary tumours have been proposed as a suitable model for aggressive human breast cancer, we identified the feline stk g...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1205221

    authors: De Maria R,Maggiora P,Biolatti B,Prat M,Comoglio PM,Castagnaro M,Di Renzo MF

    更新日期:2002-03-07 00:00:00

  • Decoding whole-genome mutational signatures in 37 human pan-cancers by denoising sparse autoencoder neural network.

    abstract::Millions of somatic mutations have recently been discovered in cancer genomes. These mutations in cancer genomes occur due to internal and external mutagenesis forces. Decoding the mutational processes by examining their unique patterns has successfully revealed many known and novel signatures from whole exome data, b...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/s41388-020-1343-z

    authors: Pei G,Hu R,Dai Y,Zhao Z,Jia P

    更新日期:2020-07-01 00:00:00

  • Estrogen-induced proliferation of normal endometrial glandular cells is initiated by transcriptional activation of cyclin D1 via binding of c-Jun to an AP-1 sequence.

    abstract::To explore the mechanism of estrogen-induced growth of normal endometrium, the transactivation system of the cyclin D1 gene was analysed using cultured normal endometrial glandular cells. Estradiol (E2) treatment of cultured normal endometrial glandular cells induced upregulation of c-Jun, and then cyclin D1 proteins,...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1207849

    authors: Shiozawa T,Miyamoto T,Kashima H,Nakayama K,Nikaido T,Konishi I

    更新日期:2004-11-11 00:00:00

  • Apoptin is modified by SUMO conjugation and targeted to promyelocytic leukemia protein nuclear bodies.

    abstract::Apoptin, a protein of the chicken anemia virus (CAV), represents a novel potential anticancer therapeutic, because it induces apoptotic death specifically in tumor but not normal cells. The cellular localization appears to be crucial for apoptin's selective toxicity. In normal cells apoptin remains in the cytoplasm, w...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1209923

    authors: Janssen K,Hofmann TG,Jans DA,Hay RT,Schulze-Osthoff K,Fischer U

    更新日期:2007-03-08 00:00:00

  • The deleted in colon cancer (DCC) gene is consistently expressed in colorectal cancers and metastases.

    abstract::The DCC (deleted in colorectal cancer) gene was originally identified as a candidate tumour suppressor gene in colon carcinogenesis on the basis of allelic losses in chromosome 18q.21 in 70% of colon cancers. Reverse transcriptase polymerase chain reaction (RT-PCR) of DCC mRNA suggests that DCC expression may also be ...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:

    authors: Gotley DC,Reeder JA,Fawcett J,Walsh MD,Bates P,Simmons DL,Antalis TM

    更新日期:1996-08-15 00:00:00

  • Targeting of the protein chaperone, HSP90, by the transformation suppressing agent, radicicol.

    abstract::Radicicol, a macrocyclic anti-fungal antibiotic, has the ability to suppress transformation by diverse oncogenes such as Src, Ras and Mos. Despite this useful property, the mechanism by which radicicol exerts its anti-transformation effects is currently unknown. To understand the transformation-suppressing effects of ...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1201790

    authors: Sharma SV,Agatsuma T,Nakano H

    更新日期:1998-05-01 00:00:00

  • The MAPK pathway functions as a redundant survival signal that reinforces the PI3K cascade in c-Kit mutant melanoma.

    abstract::Stimulation of the c-Kit receptor tyrosine kinase has a critical role in the development and migration of melanocytes, and oncogenic c-Kit mutants contribute to the progression of some melanomas. c-Kit signalling activates the mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) pathways an...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/onc.2012.562

    authors: Todd JR,Scurr LL,Becker TM,Kefford RF,Rizos H

    更新日期:2014-01-09 00:00:00

  • Identification of candidate alternative lengthening of telomeres genes by methionine restriction and RNA interference.

    abstract::Telomerase-negative cancer cells can maintain their telomeres by a recombination-mediated alternative lengthening of telomeres (ALT) process. We reported previously that sequestration of MRE11/RAD50/NBS1 complexes represses ALT-mediated telomere length maintenance, and suppresses formation of ALT-associated promyelocy...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1210260

    authors: Jiang WQ,Zhong ZH,Henson JD,Reddel RR

    更新日期:2007-07-12 00:00:00

  • Cyclin D1 overexpression combined with N-nitrosomethylbenzylamine increases dysplasia and cellular proliferation in murine esophageal squamous epithelium.

    abstract::We previously described the oral-esophageal tissue-specific expression of cyclin D1 with the Epstein-Barr virus ED-L2 promoter in transgenic mice, and resulting dysplasia. Given the evidence for an interplay between environmental and genetic factors in esophageal squamous carcinogenesis, the aim of this study was to d...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1202296

    authors: Jenkins TD,Mueller A,Odze R,Shahsafaei A,Zukerberg LR,Kent R,Stoner GD,Rustgi AK

    更新日期:1999-01-07 00:00:00

  • Down-regulation of MHC class I antigens is not a general mechanism for the increased tumorigenicity caused by c-myc amplification.

    abstract::Previous studies have shown that increased expression of oncogenes from the myc-family can down-regulate the level of MHC class I antigens in tumor cells. This has suggested a mechanism by which amplification/overexpression of myc-genes may contribute to the malignancy development of certain tumors. Earlier published ...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:

    authors: Dahllöf B

    更新日期:1990-03-01 00:00:00