KIAA1096, a Gene on Chromosome 1q, is Amplified and Overexpressed in Bladder Cancer

Huang, William C.; Taylor, S; Nguyen, Trang B.; Tomaszewski, John E.; Libertino, John A.; Malkowicz, S. Bruce; McGarvey, Terence W.

doi:10.1089/104454902760599681

Cited by 17 publications

(14 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The association of these molecules with lung cancer had not been previously reported, although, in the case of PRRC2C, there was some information suggesting its role in cancer. PRRC2C is amplified and overexpressed in bladder cancer (46), and it has been related to proliferation and cellcycle regulation through an interaction with histone H4 transcription factor (47). We have now been able to identify a new splice variant of PRRC2C, which is regulated by SRSF1 and is overexpressed in primary lung tumors.…”

Section: Discussionmentioning

confidence: 99%

Identification of Alternative Splicing Events Regulated by the Oncogenic Factor SRSF1 in Lung Cancer

et al. 2014

View full text Add to dashboard Cite

Abnormal alternative splicing has been associated with cancer. Genome-wide microarrays can be used to detect differential splicing events. In this study, we have developed ExonPointer, an algorithm that uses data from exon and junction probes to identify annotated cassette exons. We used the algorithm to profile differential splicing events in lung adenocarcinoma A549 cells after downregulation of the oncogenic serine/arginine-rich splicing factor 1 (SRSF1). Data were generated using two different microarray platforms. The PCR-based validation rate of the top 20 ranked genes was 60% and 100%. Functional enrichment analyses found a substantial number of splicing events in genes related to RNA metabolism. These analyses also identified genes associated with cancer and developmental and hereditary disorders, as well as biologic processes such as cell division, apoptosis, and proliferation. Most of the top 20 ranked genes were validated in other adenocarcinoma and squamous cell lung cancer cells, with validation rates of 80% to 95% and 70% to 75%, respectively. Moreover, the analysis allowed us to identify four genes, ATP11C, IQCB1, TUBD1, and proline-rich coiled-coil 2C (PRRC2C), with a significantly different pattern of alternative splicing in primary non-small cell lung tumors compared with normal lung tissue. In the case of PRRC2C, SRSF1 downregulation led to the skipping of an exon overexpressed in primary lung tumors. Specific siRNA downregulation of the exon-containing variant significantly reduced cell growth. In conclusion, using a novel analytical tool, we have identified new splicing events regulated by the oncogenic splicing factor SRSF1 in lung cancer. Cancer Res; 74(4); 1105-15. Ó2013 AACR.

show abstract

Section: Discussionmentioning

confidence: 99%

Identification of Alternative Splicing Events Regulated by the Oncogenic Factor SRSF1 in Lung Cancer

et al. 2014

View full text Add to dashboard Cite

show abstract

“…Finally, the hub genes SP110 (72), GALNT1 (34), and BAT2D1 (36,52) have all been linked to various cancers, including breast (SP110 and GALNT) and bladder (BAT2D1) cancers, whereby their deregulation may allow for enhanced proliferation, invasion, and evasion of apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Longitudinal system-based analysis of transcriptional responses to type I interferons

Pappas

Coppola

Gabatto

et al. 2009

Physiological Genomics

View full text Add to dashboard Cite

Type I interferons (IFNs) are pleiotropic cytokines that modulate both innate and adaptive immune responses. They have been used to treat autoimmune disorders, cancers, and viral infection and have been demonstrated to elicit differential responses within cells, despite sharing a single receptor. The molecular basis for such differential responses has remained elusive. To identify the mechanisms underlying differential type I IFN signaling, we used whole genome microarrays to measure longitudinal transcriptional events within human CD4 ϩ T cells treated with IFN-␣2b or IFN-␤1a. We identified differentially regulated genes, analyzed them for the enrichment of known promoter elements and pathways, and constructed a network module based on weighted gene coexpression network analysis (WGCNA). WGCNA uses advanced statistical measures to find interconnected modules of correlated genes. Overall, differential responses to IFN in CD4 ϩ T cells related to three dominant themes: migration, antigen presentation, and the cytotoxic response. For migration, WGCNA identified subtypespecific regulation of pre-mRNA processing factor 4 homolog B and eukaryotic translation initiation factor 4A2, which work at various levels within the cell to affect the expression of the chemokine CCL5. WGCNA also identified sterile ␣-motif domain-containing 9-like (SAMD9L) as critical in subtype-independent effects of IFN treatment. RNA interference of SAMD9L expression enhanced the migratory phenotype of activated T cells treated with IFN-␤ compared with controls. Through the analysis of the dynamic transcriptional events after differential IFN treatment, we were able to identify specific signatures and to uncover novel genes that may underpin the type I IFN response.human; T cell; cytokines; gene regulation INTERFERONS (IFNs) are pleiotropic molecules implicated in a wide range of cellular responses (44) and are Federal Drug Administration-approved therapeutics for the treatment of cancer, infection, and autoimmunity (49). Based on sequence homology and structure, IFNs are divided into three classes: types I, II, and III. Type I IFNs include IFN-␣ (15 known ␣-subtypes), IFN-␤, and IFN-, whereas type II IFN consists only of IFN-␥ and type III IFN consists only of IFN-. All type I IFNs activate a common cell surface receptor [the IFN receptor (IFNR)], which exists as two separate polypeptides (IFNAR1 and IFNAR2) with no intrinsic dimerization capacity (12). Binding of type I IFNs to IFNAR2, recruitment of IFNAR1, and stabilization of a heterotrimeric ligand/receptor complex activate members of the Jak1/tyrosine kinase 2 (Tyk2) and JAK/STAT pathways (12, 45). Phosphorylated STAT1/ STAT2 heterodimers form transcriptional activation complexes with IFN regulatory factor (IRF)9/p48, translocate to the nucleus, and drive the expression of numerous genes, including myxovirus resistance protein 1 (MX1), 2Ј,5Ј-oligoadenylate synthetase 1, and double-stranded RNA-activated protein kinase (EIF2AK2).Although type I IFNs share the same cognate receptor and und...

show abstract

“…So some new markers should be found. The Cks1 gene is located at chromosome 1q21, a region that is commonly overrepresented in breast cancer (Orsetti et al 2006), prostate cancer (Valeri et al 1999), and bladder cancer (Huang et al 2002). The Cks1 protein is a member of the highly conserved family of Cks/Suc1 proteins which interact with Cdks and was found to be an essential cofactor for eYcient Skp2-dependent ubiquitination of p27.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Overexpression of Cks1 is associated with poor survival by inhibiting apoptosis in breast cancer

Wang¹,

Tian²,

Tian

et al. 2009

J Cancer Res Clin Oncol

View full text Add to dashboard Cite

show abstract

KIAA1096, a Gene on Chromosome 1q, is Amplified and Overexpressed in Bladder Cancer

Cited by 17 publications

References 11 publications

Identification of Alternative Splicing Events Regulated by the Oncogenic Factor SRSF1 in Lung Cancer

Identification of Alternative Splicing Events Regulated by the Oncogenic Factor SRSF1 in Lung Cancer

Longitudinal system-based analysis of transcriptional responses to type I interferons

RETRACTED ARTICLE: Overexpression of Cks1 is associated with poor survival by inhibiting apoptosis in breast cancer

Contact Info

Product

Resources

About