Cloning and molecular characterization of a novel gene strongly induced by the adenovirus E1A gene in rat thyroid cells

Visconti, Roberta; Schepis, Filippo; Iuliano, Rodolfo; Pierantoni, Giovanna Maria; Zhang, Li; Carlomagno, Francesca; Battaglia, C; Martelli, Marialuisa; Trapasso, Francesco; Santoro, Massimo; Fusco, Alfredo

doi:10.1038/sj.onc.1206194

Cited by 56 publications

(28 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Until today, investigation of the Dro1 tumor suppressor function in vivo was restricted to expression analysis, offering evidence for involvement in colorectal, mammary, and thyroid carcinogenesis (9,10,18,19). The results of the present study clearly demonstrate Dro1 to be an important colonic tumor suppressor gene in vivo that suppresses polyp initiation and particularly prevents tumor progression toward malignancy in Apc Min/þ mice.…”

Section: Discussionmentioning

confidence: 49%

See 1 more Smart Citation

DRO1 Inactivation Drives Colorectal Carcinogenesis in ApcMin/+ Mice

Grill

Neumann

Herbst

et al. 2014

Molecular Cancer Research

View full text Add to dashboard Cite

Colorectal cancer develops from adenomatous precursor lesions by a multistep process that involves several independent mutational events in oncogenes and tumor suppressor genes. Inactivation of the adenomatous polyposis coli (APC) tumor suppressor gene is an early event and a prerequisite for the development of human colorectal adenoma. Previous in vitro studies identified DRO1 (CCDC80) to be a putative tumor suppressor gene that is negatively regulated in colorectal cancers and downregulated upon neoplastic transformation of epithelial cells. To investigate the in vivo role of DRO1 in colorectal carcinogenesis, a constitutive DRO1 knockout mouse model was generated. Disruption of DRO1 did not result in spontaneous intestinal tumor formation, consistent with the notion that DRO1 might have a role in suppressing the development of colon tumors in Apc Min/þ mice, a widely used model for studying the role of APC in intestinal tumorigenesis that is hampered by the fact that mice predominantly develop adenomas in the small intestine and not in the colon. Here, deletion of DRO1 in ApcMin/þ mice results in earlier death, a dramatically increased colonic tumor burden, and frequent development of colorectal carcinoma. Furthermore, enhanced phosphorylation of ERK1/2 is observed in colon epithelium and tumors from DRO1 knockout mice. Thus, this study reveals that inactivation of DRO1 is required for colorectal carcinogenesis in the Apc Min/þ mouse and establishes a new mouse model for the study of colorectal cancer.

show abstract

Section: Discussionmentioning

confidence: 49%

“…The expression of DRO1 has been found to be reduced in human cancers, including colorectal and thyroid tumors (9,10). We found DRO1 to suppress anchorage-independent growth and to sensitize cancer cells to detachmentinduced apoptosis (anoïkis).…”

Section: Introductionmentioning

confidence: 78%

DRO1 Inactivation Drives Colorectal Carcinogenesis in ApcMin/+ Mice

Grill

Neumann

Herbst

et al. 2014

Molecular Cancer Research

View full text Add to dashboard Cite

show abstract

“…Ubiquitous tissue distribution has also been observed for the zebrafisch; however, here, maximum expression locates to the heart [21]. In rat and mouse, Dro1/Ccdc80 is expressed as a single transcript [8,25]. However, in human and chicken, two alternative forms of DRO1/CCDC80 transcripts have been described [8,11,[25][26][27] of which the larger one is expressed more abundantly in human tissue [8,25,27].…”

Section: Expression Pattern Of Dro1/ccdc80mentioning

confidence: 67%

“…However, in human and chicken, two alternative forms of DRO1/CCDC80 transcripts have been described [8,11,[25][26][27] of which the larger one is expressed more abundantly in human tissue [8,25,27]. Interestingly, for human tissue, controversial results concerning the size of the transcripts have been obtained (4.2 and 3.8 kb [8] [26]). In chicken, the two forms of transcripts, termed Equarin-L (4.2 kb) and Equarin-S (3.9 kb), have been suggested to be alternatively spliced variants of DRO1/CCDC80 [11].…”

Section: Expression Pattern Of Dro1/ccdc80mentioning

confidence: 90%

“…Now, the official name of the gene is CCDC80 for coiled-coil domain containing 80. Independently, sequences of the coding region of mouse Dro1/Ccdc80 have been cloned as an estrogen-regulated gene, steroid-sensitive gene 1 (SSG1), from rat uterus and mammary gland [9], as URB (upregulated in bombesin receptor subtype-3 (BRS-3)-deficient mice) from adipose tissue of obese BRS-3-deficient mice [19], cloned as CL2 (clone 2) from rat thyroid PC CL3 cells following transformation by the adenovirus E1A gene [8], and as Equarin from the chicken embryonic lens [11]. O'Leary et al recloned Dro1/Ccdc80 alias SSG1/Ccdc80 from a rat adipose cDNA library [20•], and recently, molecular cloning of the zebrafish Dro1/Ccdc80 homolog has been obtained [21].…”

Section: Cloning Of Dro1/ccdc80mentioning

confidence: 99%

See 1 more Smart Citation

DRO1/CCDC80: a Novel Tumor Suppressor of Colorectal Carcinogenesis

Grill

Kolligs

2015

Curr Colorectal Cancer Rep

View full text Add to dashboard Cite

Dro1/Ccdc80 has been identified as a tumor suppressor gene in colorectal, thyroid, and ovarian cancer. Dro1/ Ccdc80 is ubiquitously expressed and has, next to its tumor suppressive role, been implicated in a wide range of biological processes, including adipogenesis, lens development, and skeletogenesis. DRO1/CCDC80 is a secreted protein that assembles with the extracellular matrix and promotes cell adhesion. The biological mechanisms by which DRO1/CCDC80 exerts its various functions are still widely unknown. DRO1/ CCDC80 inhibits malignant growth properties of cancer cells, mediates sensitization to apoptosis, regulates E-cadherin expression, and acts as a binding partner for Janus kinase 2 and cyclic GMP-dependent protein kinase 1. Moreover, DRO1 has been linked to MEK/ERK, fibroblast growth factor (FGF), Hedgehog, and Wnt/β-catenin signaling. In the following, DRO1/CCDC80 is presented as a novel tumor suppressor of colorectal carcinogenesis.

show abstract

The Coiled‐Coil Domain Containing 80 (ccdc80) Gene Regulates gadd45β2 Expression in the Developing Somites of Zebrafish as a New Player of the Hedgehog Pathway

Noce

Carra

Brusegan

et al. 2014

Journal Cellular Physiology

Self Cite

View full text Add to dashboard Cite

The Coiled-Coil Domain Containing 80 (CCDC80) gene has been identified as strongly induced in rat thyroid PC CL3 cells immortalized by the adenoviral E1A gene. In human, CCDC80 is a potential oncosoppressor due to its down-regulation in several tumor cell lines and tissues and it is expressed in almost all tissues. CCDC80 has homologous in mouse, chicken, and zebrafish. We cloned the zebrafish ccdc80 and analyzed its expression and function during embryonic development. The in-silico translated zebrafish protein shares high similarity with its mammalian homologous, with nuclear localization signals and a signal peptide. Gene expression analysis demonstrates that zebrafish ccdc80 is maternally and zygotically expressed throughout the development. In particular, ccdc80 is strongly expressed in the notochord and it is under the regulation of the Hedgehog pathway. In this work we investigated the functional effects of ccdc80-loss-of-function during embryonic development and verified its interaction with gadd45β2 in somitogenesis.

show abstract

Cloning and molecular characterization of a novel gene strongly induced by the adenovirus E1A gene in rat thyroid cells

Cited by 56 publications

References 47 publications

DRO1 Inactivation Drives Colorectal Carcinogenesis in ApcMin/+ Mice

DRO1 Inactivation Drives Colorectal Carcinogenesis in ApcMin/+ Mice

DRO1/CCDC80: a Novel Tumor Suppressor of Colorectal Carcinogenesis

The Coiled‐Coil Domain Containing 80 (ccdc80) Gene Regulates gadd45β2 Expression in the Developing Somites of Zebrafish as a New Player of the Hedgehog Pathway

Contact Info

Product

Resources

About