<i>TCEB1</i> promotes invasion of prostate cancer cells

Jalava, Sanni E.; Porkka, Kati P.; Rauhala, Hanna E.; Isotalo, Jarkko; Tammela, Teuvo L.J.; Visakorpi, Tapio

doi:10.1002/ijc.23916

Cited by 31 publications

(27 citation statements)

References 38 publications

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“…Like Elongin A and VHL, Elongin A3 possesses the Elongin C binding sequence and can form a putative ubiquitylation complex with Elongin BC and Cul5/Rbx2 (Yamazaki et al 2002). Interestingly, Elongin C (TCEB1) has been shown to be overexpressed and to promote invasion of prostate cancer cells (Jalava et al 2009) metastatic SI-NETs, using a variety of techniques, such as LOH, CGH, CGH-array, SNP analysis, and SNP-array (Kytola et al 2001, Löllgen et al 2001, Tonnies et al 2001, Stancu et al 2003, Wang et al 2005, Kim do et al 2008, Kulke et al 2008, Andersson et al 2009, Cunningham et al 2011, Walsh et al 2011. Perhaps the most conspicuous finding is the observation of frequent loss of one copy of the whole chromosome.…”

Section: Discussionmentioning

confidence: 99%

TCEB3C a putative tumor suppressor gene of small intestinal neuroendocrine tumors

Edfeldt

Ahmad

Åkerström

et al. 2013

Endocrine-Related Cancer

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Small intestinal neuroendocrine tumors (SI-NETs), formerly known as midgut carcinoids, are rare and slow-growing neoplasms. Frequent loss of one copy of chromosome 18 in primary tumors and metastases has been observed. The aim of the study was to investigate a possible role of TCEB3C (Elongin A3), currently the only imprinted gene on chromosome 18, as a tumor suppressor gene in SI-NETs, and whether its expression is epigenetically regulated. Primary tumors, metastases, the human SI-NET cell line CNDT2.5, and two other cell lines were included. Immunohistochemistry, gene copy number determination by PCR, colony formation assay, western blotting, real-time quantitative RT-PCR, RNA interference, and quantitative CpG methylation analysis by pyrosequencing were performed. A large majority of tumors (33/43) showed very low to undetectable Elongin A3 expression and as expected 89% (40/45) displayed one gene copy of TCEB3C. The DNA hypomethylating agent 5-aza-2 0 -deoxycytidine induced TCEB3C expression in CNDT2.5 cells, in primary SI-NET cells prepared directly after surgery, but not in two other cell lines. Also siRNA to DNMT1 and treatment with the general histone methyltransferase inhibitor 3-deazaneplanocin A induced TCEB3C expression in a cell type-specific way. CpG methylation at the TCEB3C promoter was observed in all analyzed tissues and thus not related to expression. Overexpression of TCEB3C resulted in a 50% decrease in clonogenic survival of CNDT2.5 cells, but not of control cells. The results support a putative role of TCEB3C as a tumor suppressor gene in SI-NETs. Epigenetic repression of TCEB3C seems to be tumor cell type-specific and involves both DNA and histone methylation.

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Section: Discussionmentioning

confidence: 99%

TCEB3C a putative tumor suppressor gene of small intestinal neuroendocrine tumors

Edfeldt

Ahmad

Åkerström

et al. 2013

Endocrine-Related Cancer

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“…Western blotting Cytoplasmic and nuclear proteins were isolated as described previously (Jalava et al, 2009). Briefly, proteins were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis using 12% (BTG2), 10% (PIK3IP1) or 15% (BIM) polyacrylamide gels and transferred to polyvinylidene fluoride membranes (Immobilon-P, Millipore Corp., Billerica, MA, USA).…”

Section: Cell Cycle Analysismentioning

confidence: 99%

Androgen-regulated miR-32 targets BTG2 and is overexpressed in castration-resistant prostate cancer

et al. 2012

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Evaluation of Cellular Determinants Required for In Vitro Xenotropic Murine Leukemia Virus-Related Virus Entry into Human Prostate Cancer and Noncancerous Cells

Bhosle¹,

Suppiah²,

Molinaro³

et al. 2010

J Virol

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Prostate cancer is the most common male malignancy in Western countries and the second most common cause of cancer-related deaths in males worldwide (15,24). The known risk factors for prostate cancer are hormones (i.e., androgens), diet, sex, and race, as well as environmental and genetic factors (27). A recent study suggests that susceptibility to prostate cancer can be influenced by the genetic variations associated with an antagonistic coevolution, which occurs between a specific host locus (RNASEL), known to be involved in antiviral innate immune defense, and a viral pathogen (38). Indeed, several epidemiologic studies have supported the involvement of the RNASEL gene in the prostate cancer etiology (4,5,30,31), whereas other studies do not (9,22,34,43). Some studies have reported that individuals with a single mutated copy of the RNASEL gene have a 50% increased risk for prostate cancer, whereas those with homozygous mutant RNASEL alleles have a 2-fold-increased risk of prostate cancer (5).The RNASEL gene encodes for the RNase L protein, a constitutively expressed latent endoribonuclease, which mediates the interferon-inducible 2-5A system against viral and/or cellular double-stranded RNAs (8,16,20,23,49,50). The RNase L "Q" variant allele (R462Q) shows a 3-fold decrease in catalytic activity compared to the wild-type enzyme (5, 44). The possible association of mutant RNASEL alleles with human prostate cancers suggests an enhanced susceptibility of prostate tissues to a viral agent. This hypothesis has led to the recent identification of a new human retrovirus, xenotropic murine leukemia virus (MuLV)-related virus (XMRV), in 40% of prostate cancer patients with the QQ variant alleles of RNASEL compared to 1.5% among heterozygous (RQ) and wild-type (RR) RNASEL carriers (41). XMRV virus infection appears to be susceptible to inhibition by interferon and its downstream effector RNase L protein (7). However, a recent study has provided some evidence to show that XMRV infection is independent of the RNASEL genotype (34), suggesting that population differences and/or other environmental or genetic factors may influence the impact of RNASEL on prostate cancer development.The XMRV genome is 8,185 nucleotides in length and shares up to 95% overall nucleotide sequence identity with known xenotropic MuLVs (41). One receptor for xenotropic MuLVs is Xpr1, a 696-amino-acid protein with multiple transmembrane-spanning domains (2). Expression of this protein in Chinese hamster ovary (CHO) cells that are not known to express Xpr1 endogenously confers an enhanced susceptibility of these cells to xenotropic MuLV infection (2). Infection of hamster and mouse cells with XMRV-like virus that is derived from a prostate cancer cell line (22Rv1) also requires Xpr1 as a receptor (18). Earlier studies have demonstrated the importance of certain residues located within the putative third and fourth extracellular loops (ECL3 and ECL4) of Mus dunni's Xpr1 in conferring infection by xenotropic MuLVs (25). Furthermore, it has been shown ...

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TCEB1 promotes invasion of prostate cancer cells

Cited by 31 publications

References 38 publications

TCEB3C a putative tumor suppressor gene of small intestinal neuroendocrine tumors

TCEB3C a putative tumor suppressor gene of small intestinal neuroendocrine tumors

Androgen-regulated miR-32 targets BTG2 and is overexpressed in castration-resistant prostate cancer

Evaluation of Cellular Determinants Required for In Vitro Xenotropic Murine Leukemia Virus-Related Virus Entry into Human Prostate Cancer and Noncancerous Cells

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