Overexpression of miR-17-5p may negatively impact p300/CBP factor-associated inflammation in a hypercholesterolemic advanced prostate cancer model

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Citações na Scopus
1
Tipo de produção
article
Data de publicação
2023
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ISSN da Revista
Título do Volume
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SPRINGER
Citação
MOLECULAR BIOLOGY REPORTS, v.50, n.9, p.7333-7345, 2023
Projetos de Pesquisa
Unidades Organizacionais
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Resumo
BackgroundPreviously, we demonstrated that cholesterol triggers the increase in p300/CBP-associated factor (PCAF), targeted by miR-17-5p. The p300, IL-6, PCAF, and miR-17-5p genes have important and contradictory roles in inflammation and prostate cancer (PCa). This study aimed to demonstrate the potential anti-inflammatory effect of miR-17-5 in an advanced PCa model with diet-induced hypercholesterolemia.Methods and resultsIn vitro, using the PC-3 cell line, we show that induction of miR-17-5p reduces p300 and PCAF expression, increases apoptosis, and decreases cell migration. Furthermore, we demonstrate that supplementing this same cell with cholesterol (2 & mu;g/mL) triggers increased p300, IL-6, and PCAF. In vivo, after establishing the hypercholesterolemic (HCOL) model, xenografts were treated with miR-17-5p. Increased expression of this miR after intratumoral injections attenuated tumor growth in the control and HCOL animals and reduced cell proliferation.ConclusionOur results demonstrate that inducing miR-17-5p expression suppresses tumor growth and inflammatory mediator expression. Further studies should be conducted to fully explore the role of miR-17-5p and the involvement of inflammatory mediators p300, PCAF, and IL-6.
Palavras-chave
Prostate cancer, MicroRNA, Inflammation, IL-6, p300
Referências
  1. Chen TS, 2000, CANCER RES, V60, P2132
  2. Chmelar R, 2007, INT J CANCER, V120, P719, DOI 10.1002/ijc.22365
  3. Cho HJ, 2015, NUTRIENTS, V7, P2539, DOI 10.3390/nu7042539
  4. Chung S, 2019, INT J MOL SCI, V20, DOI 10.3390/ijms20071554
  5. Coucha M, 2017, WORLD J DIABETES, V8, P56, DOI 10.4239/wjd.v8.i2.56
  6. de Jong RCM, 2017, PLOS ONE, V12, DOI 10.1371/journal.pone.0185820
  7. Debes JD, 2002, CANCER RES, V62, P5632
  8. Gang XK, 2016, ONCOTARGET, V7, P15135, DOI 10.18632/oncotarget.7715
  9. Gathirua-Mwangi WG, 2014, EUR J CANCER PREV, V23, P96, DOI 10.1097/CEJ.0b013e3283647394
  10. Ghizzoni M, 2010, BIOORGAN MED CHEM, V18, P5826, DOI 10.1016/j.bmc.2010.06.089
  11. Gong AY, 2012, BMC CANCER, V12, DOI 10.1186/1471-2407-12-492
  12. Hanahan D, 2011, CELL, V144, P646, DOI 10.1016/j.cell.2011.02.013
  13. Hayashi T, 2018, CLIN CANCER RES, V24, P4309, DOI 10.1158/1078-0432.CCR-18-0106
  14. Hobisch A, 1998, CANCER RES, V58, P4640
  15. Huang J, 2015, EPIGENETICS-US, V10, P62, DOI 10.4161/15592294.2014.990780
  16. Jin LY, 2017, CANCER RES, V77, P5564, DOI 10.1158/0008-5472.CAN-17-0314
  17. Lavery DN, 2011, J BIOMED BIOTECHNOL, DOI 10.1155/2011/862125
  18. Lumeng CN, 2007, DIABETES, V56, P16, DOI 10.2337/db06-1076
  19. MINISTERIO DA SAUDE-Instituto Nacional de Cancer Jose Alencar Gomes da Silva (INCA), 2018, EST 2018 INC CANC BR
  20. Nguyen DP, 2014, BJU INT, V113, P986, DOI 10.1111/bju.12452
  21. Pimenta Ruan, 2022, Cell Physiol Biochem, V56, P1, DOI 10.33594/000000592
  22. Qiu LQ, 2019, BIOCHEM BIOPH RES CO, V513, P41, DOI 10.1016/j.bbrc.2019.03.157
  23. Sikand K, 2009, CANCER CELL INT, V9, DOI 10.1186/1475-2867-9-21
  24. Smidowicz A, 2015, ADV NUTR, V6, P738, DOI 10.3945/an.115.009415
  25. Stoen MJ, 2021, SCI REP-UK, V11, DOI 10.1038/s41598-021-93208-6
  26. Thapa D, 2014, CANCER RES, V74, P5644, DOI 10.1158/0008-5472.CAN-14-0562
  27. Wu K, 2016, INT J CANCER, V138, P2368, DOI 10.1002/ijc.29973
  28. Zhang T, 2016, NAT COMMUN, V7, DOI 10.1038/ncomms11674
  29. Zhang XP, 2009, CLIN EXP METASTAS, V26, P965, DOI 10.1007/s10585-009-9287-2