The expression of RNA helicase DDX5 is transcriptionally upregulated by calcitriol through a vitamin D response element in the proximal promoter in SiHa cervical cells

详细信息    查看全文

• 作者：Ramiro José González-Duarte ; Verna Cázares-Ordo?ez…
• 关键词：Vitamin D ; RNA helicase ; Nuclear receptor ; VDR ; Cervical cancer
• 刊名：Molecular and Cellular Biochemistry
• 出版年：2015
• 出版时间：December 2015
• 年：2015
• 卷：410
• 期：1-2
• 页码：65-73
• 全文大小：1,906 KB
• 参考文献：1.Fuller-Pace FV, Moore HC (2011) RNA helicases p68 and p72: multifunctional proteins with important implications for cancer development. Future Oncol 7:239-51CrossRef PubMed
  2.Jung C, Mittler G, Oswald F, Borggrefe T (2013) RNA helicase Ddx5 and the noncoding RNA SRA act as coactivators in the Notch signaling pathway. Biochim Biophys Acta 1833:1180-189CrossRef PubMed
  3.Warner DR, Bhattacherjee V, Yin X, Singh S, Mukhopadhyay P, Pisano MM, Greene RM (2004) Functional interaction between Smad, CREB binding protein, and p68 RNA helicase. Biochem Biophys Res Commun 324:70-6CrossRef PubMed
  4.Clark EL, Fuller-Pace FV, Elliott DJ, Robson CN (2008) Coupling transcription to RNA processing via the p68 DEAD box RNA helicase androgen receptor co-activator in prostate cancer. Biochem Soc Trans 36:546-47CrossRef PubMed
  5.Wagner M, Rid R, Maier CJ, Maier RH, Laimer M, Hintner H, Bauer JW, Onder K (2012) DDX5 is a multifunctional co-activator of steroid hormone receptors. Mol Cell Endocrinol 361:80-1CrossRef PubMed
  6.Bates GJ, Nicol SM, Wilson BJ, Jacobs AM, Bourdon JC, Wardrop J, Gregory DJ, Lane DP, Perkins ND, Fuller-Pace FV (2005) The DEAD box protein p68: a novel transcriptional coactivator of the p53 tumour suppressor. EMBO J 24:543-53PubMedCentral CrossRef PubMed
  7.Caretti G, Schiltz RL, Dilworth FJ, Di Padova M, Zhao P, Ogryzko V, Fuller-Pace FV, Hoffman EP, Tapscott SJ, Sartorelli V (2006) The RNA helicases p68/p72 and the noncoding RNA SRA are coregulators of MyoD and skeletal muscle differentiation. Dev Cell 11:547-60CrossRef PubMed
  8.Jensen ED, Niu L, Caretti G, Nicol SM, Teplyuk N, Stein GS, Sartorelli V, van Wijnen AJ, Fuller-Pace FV, Westendorf JJ (2008) p68 (Ddx5) interacts with Runx2 and regulates osteoblast differentiation. J Cell Biochem 103:1438-451CrossRef PubMed
  9.Wang R, Jiao Z, Li R, Yue H, Chen L (2012) p68 RNA helicase promotes glioma cell proliferation in vitro and in vivo via direct regulation of NF-kappaB transcription factor p50. Neuro Oncol 14:1116-124PubMedCentral CrossRef PubMed
  10.Jalal C, Uhlmann-Schiffler H, Stahl H (2007) Redundant role of DEAD box proteins p68 (Ddx5) and p72/p82 (Ddx17) in ribosome biogenesis and cell proliferation. Nucleic Acids Res 35:3590-601PubMedCentral CrossRef PubMed
  11.Rossler OG, Straka A, Stahl H (2001) Rearrangement of structured RNA via branch migration structures catalysed by the highly related DEAD-box proteins p68 and p72. Nucleic Acids Res 29:2088-096PubMedCentral CrossRef PubMed
  12.Saporita AJ, Chang HC, Winkeler CL, Apicelli AJ, Kladney RD, Wang J, Townsend RR, Michel LS, Weber JD (2011) RNA helicase DDX5 is a p53-independent target of ARF that participates in ribosome biogenesis. Cancer Res 71:6708-717PubMedCentral CrossRef PubMed
  13.Liu ZR (2002) p68 RNA helicase is an essential human splicing factor that acts at the U1 snRNA-5-splice site duplex. Mol Cell Biol 22:5443-450PubMedCentral CrossRef PubMed
  14.Zonta E, Bittencourt D, Samaan S, Germann S, Dutertre M, Auboeuf D (2013) The RNA helicase DDX5/p68 is a key factor promoting c-fos expression at different levels from transcription to mRNA export. Nucleic Acids Res 41:554-64PubMedCentral CrossRef PubMed
  15.Carlberg C, Campbell MJ (2013) Vitamin D receptor signaling mechanisms: integrated actions of a well-defined transcription factor. Steroids 78:127-36CrossRef PubMed
  16.Giangreco AA, Nonn L (2013) The sum of many small changes: microRNAs are specifically and potentially globally altered by vitamin D3 metabolites. J Steroid Biochem Mol Biol 136:86-3PubMedCentral CrossRef PubMed
  17.González-Duarte RJ, Cázares-Ordo?ez V, Romero-Córdoba S, Díaz L, Ortíz V, Freyre-González JA, Hidalgo-Miranda A, Larrea F, Avila E (2015) Calcitriol increases Dicer expression and modifies the microRNAs signature in SiHa cervical cancer cells. Biochem Cell Biol 93:376-84CrossRef PubMed
  18.Avila E, Garcia-Becerra R, Rodriguez-Rasgado JA, Diaz L, Ordaz-Rosado D, Zugel U, Steinmeyer A, Barrera D, Halhali A, Larrea F, Camacho J (2010) Calcitriol down-regulates human ether a go-go 1 potassium channel expression in cervical cancer cells. Anticancer Res 30:2667-672PubMed
  19.Cázares-Ordo?ez V, Gonzalez-Duarte RJ, Diaz L, Ishizawa M, Uno S, Ortiz V, Ordonez-Sanchez ML, Makishima M, Larrea F, Avila E (2015) A cis-acting element in the promoter of human ether a go-go 1 potassium channel gene mediates repression by calcitriol in human cervical cancer cells. Biochem Cell Biol 93:94-01CrossRef PubMed
  20.Rossler OG, Hloch P, Schutz N, Weitzenegger T, Stahl H (2000) Structure and expression of the human p68 RNA helicase gene. Nucleic Acids Res 28:932-39PubMedCentral CrossRef PubMed
  21.Untergasser A, Cutcutache I, Koressaar T, Ye J, Faircloth BC, Remm M, Rozen SG (2012) Primer3—new capabilities and interfaces. Nucleic Acids Res 40:e115PubMedCentral CrossRef PubMed
  22.Cartharius K, Frech K, Grote K, Klocke B, Haltmeier M, Klingenhoff
• 作者单位：Ramiro José González-Duarte (1) (3)
  Verna Cázares-Ordo?ez (1) (3)
  Lorenza Díaz (1)
  Víctor Ortíz (2)
  Fernando Larrea (1)
  Euclides Avila (1)
  
  1. Department of Reproductive Biology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Vasco de Quiroga # 15, Col. Sección XVI, 14080, Mexico, D.F., Mexico
  3. School of Medicine, Universidad Nacional Autónoma de México, Circuito Interior, Ciudad Universitaria, Av. Universidad # 3000, 04510, Mexico, D.F., Mexico
  2. Department of Physiology of Nutrition, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Vasco de Quiroga # 15, Col. Sección XVI, 14080, Mexico, D.F., Mexico
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Life Sciences
  Biochemistry
  Medical Biochemistry
  Oncology
  Cardiology
  
• 出版者：Springer Netherlands
• ISSN：1573-4919

文摘

The DEAD box RNA helicase DDX5 is a multifunctional protein involved in the regulatory events of gene expression. Herein, we presented evidence indicating that DDX5 is transcriptionally upregulated by calcitriol, the hormonal form of vitamin D₃. In silico analysis revealed the presence of two putative vitamin D response elements (VDREs) in the DDX5 promoter region. Using luciferase reporter assays, we demonstrated that the DDX5 promoter containing these putative VDREs significantly increased the luciferase activity in vitamin D receptor (VDR)-positive SiHa cells upon calcitriol treatment. Electrophoretic mobility shift assays showed the ability of VDR and retinoid X receptor to interact only with the most proximal VDRE, while chromatin immunoprecipitation analysis confirmed the occupancy of this VDRE by the VDR. Finally, we demonstrated that calcitriol significantly increased both DDX5 mRNA and protein in SiHa cells. In summary, this study shows that DDX5 gene is transcriptionally upregulated by calcitriol through a VDRE located in its proximal promoter. Given the importance of DDX5 as a master regulator of differentiation programs, our study suggests that the pro-differentiating properties of calcitriol may be related with the induction of DDX5. Keywords Vitamin D RNA helicase Nuclear receptor VDR Cervical cancer