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OVER KANSERİ HÜCRELERİNDE PRİMA-1 Met TEDAVİSİNE YANIT OLARAK DEĞİŞEN miRNA EKSPRESYON ANALİZİ

Yıl 2020, , 19 - 25, 04.05.2020
https://doi.org/10.34108/eujhs.543409

Öz

Tümör hücrelerinde p53
fonksiyonunun restorasyonu, over kanseri tedavisinde çekici bir strateji olacağı
düşünülmektedir, çünkü p53 mutasyonlarının over kanserlerinde görülme
sıklığı  %50-60 arasındadır. Küçük
molekül Prima-1Met'in, p53'ün tümör baskılama fonksiyonunu geri
kazandığı ve insan tümör hücrelerinde hücre
büyümesini inhibe ettiği ve
apoptozu indüklediği gösterilmiştir. MikroRNA'lar hem transkripsiyonel hem de translasyonel
seviyelerde gen ekspresyonunu düzenler ve hücre proliferasyonu, farklılaşma ve
hematopoez gibi çok çeşitli fizyolojik ve biyolojik süreçlerde etki yapar.
Epitelyal over kanserinde yapılan çok sayıdaki miRNA profillemesi
çalışmalarında, kemoterapi direnci ve hastalık progresyonu ile ilişkili
miRNA'lar tanımlanmıştır, fakat, Prima-1Met'e yanıt olarak
miRNA'ların tutulumu hakkında çok az şey bilinmektedir. Bu çalışmada,
apoptotik
etkisi olduğu bilinen Prima-1Met ile
muamele edilmiş over kanseri hücre hatlarında, bu ilaca yanıt olarak
ekspresyonu değişen miRNA’ların belirlenmesini hedeflendi ve bunun için ilaç
verilen hücre hatlarında hem kanser hem de apoptosis yolaklarını hedefleyen
miRNA’ların ekspresyonları miScript PCR array ile belirlenip analiz edilmiştir.
Analiz sonucunda,
her iki hücre hattında da hem over kanseri hem de
apoptosisle ilişkili olarak Prima-1Metuygulamasıyla
ekspresyonu artan miRNA’lar; miRNA-1, miRNA-134, miRNA-141, miRNA-143,
miRNA-145, miRNA-204, miRNA-205, miRNA-214, miRNA-29a ve miRNA-29c olarak
belirlenmiştir. Ekspresyonu azalan miRNA’lar ise miRNA-21, miRNA-221 ve
miRNA-222 olarak tespit edilmiştir. Bu çalışma Prima-1Met indüklü
apoptosisin moleküler mekanizmasının aydınlatılması için bir temel
oluşturmaktadır. 




Kaynakça

  • 1. Sankaranarayanan R and Ferlay J: Worldwide burden of gynaecological cancer: The size of the problem. Best Pract Res Clin Obstet Gynaecol 20: 207-225, 2006.
  • 2. Levine AJ. p53, the cellular gatekeeper for growth and division. Cell 88: 323-331, 1997.
  • 3. Vogelstein B, Lane D, Levine AJ. Surfing the p53 network. Nature 408: 307-310, 2000.
  • 4. El-Hizawi S, Lagowski JP, Kulesz-Martin M, Albor A. Induction of gene amplification as a gain-offunction phenotype of mutant p53 proteins. Cancer Res 62: 3264-3270, 2002.
  • 5. Teneriello MG, Ebina M, Linnoila Rl, Henry M, Nash JD, Park RC, et al: p53 and Ki-ras gene mutations in epithelial ovarian neoplasms. Cancer Research 1993, 53:3103-8.
  • 6. Mazare R, Pujol P, Maudelonde T, Jeanteur P, Theillet C: p53 mutations in ovarian cancer: a late event? Oncogene 1991,6:1685-90.
  • 7. Eccles DM, Brett L, Lessells A, Gruber L, Lane D, Steel CM, et al: Overexpression of the p53 protein and allele loss at 17p13 in ovarian carcinoma. Br J Cancer 1992, 65:40-4.
  • 8. Kohler MF, Kerns BJ, Humphrey PA, Marks JR, Bast RC, Berchuck A: Mutation and overexpression of p53 in earlystage epithelial ovarian cancer. Obstet Gynecol 1993, 81:643-50.
  • 9. Hoe KK, Verma CS, Lane DP. Drugging the p53 pathway: understanding the route to clinical efficacy. Nat Rev Drug Discov 13: 217–36, 2014.
  • 10. Bykov VJ, Issaeva N, Shilov A, Hultcrantz M, Pugacheva E, Chumakov P, et al. Restoration of the tumor suppressor function to mutant p53 by a low molecular-weight compound. Nat Med 8: 282–8, 2002.
  • 11. Bykov VJ, Zache N, Stridh H, Westman J, Bergman J, Selivanova G, et al. PRIMA-1MET synergizes with cisplatin to induce tumor cell apoptosis. Oncogene 24: 3484–91, 2005.
  • 12. Bykov VJ, Issaeva N, Selivanova G, Wiman KG. Mutant p53-dependent growth suppression distinguishes PRIMA-1 from known anticancer drugs: a statistical analysis of information in the National Cancer Institute database. Carcinogenesis 23: 2011–8, 2002.
  • 13. Shi H, Lambert JM, Hautefeuille A, Bykov VJ, Wiman KG, Hainaut P, et al. In vitro and in vivo cytotoxic effects of PRIMA-1 on hepatocellular carcinoma cells expressing mutant p53ser249. Carcinogenesis 29: 1428–34, 2008.
  • 14. Liang Y, Besch-Williford C, Hyder SM. PRIMA-1 inhibits growth of breast cancer cells by re-activating mutant p53 protein. Int J Oncol 35: 1015–23, 2009.
  • 15. Zandi R, Selivanova G, Christensen CL, Gerds TA, Willumsen BM, Poulsen HS. PRIMA-1Met/APR-246 induces apoptosis and tumor growth delay in small cell lung cancer expressing mutant p53. Clin Cancer Res 17: 2830–41, 2011.
  • 16. Zache N, Lambert JM, Wiman KG, Bykov VJ. PRIMA-1MET inhibits growth of mouse tumors carrying mutant p53. Cell Oncol 30: 411–8, 2008.
  • 17. Liang Y, Besch-Williford C, Benakanakere I, Hyder SM. Re-activation of the p53 pathway inhibits in vivo and in vitro growth of hormone-dependent human breast cancer cells. Int J Oncol 31: 777–84, 2007.
  • 18. Synnott N, Pierce A, Mullooly M, Caiazza F, McGowan PM, O’Donovan N, et al. Mutant p53: a therapeutic target for the treatment of triple-negative breast cancer? J Clin Oncol 32(5s) [suppl; abstr 1118], 2014.
  • 19. Bartel DP. MicroRNAs: genomics, biogenesis, mechanism, function. Cell 116:281–297, 2004.
  • 20. Ambros V. The functions of animal microRNAs. Nature 431:350–355, 2004.
  • 21. Zhang B, Pan X, Cobb GP, Anderson TA. microRNAs as oncogenes and tumor suppressors. Dev Biol. 302:1–12, 2007.
  • 22. Yang, D. et al. Intregrated analyses identify a master microRNA regulatory network for the mesenchymal subtype in serous ovarian cancer. Cancer Cell 23: 186–199, 2013.
  • 23. Kumar, M. S., Lu, J., Mercer, K. L., Golub, T. R. & Jacks, T. Impaired microRNA processing enhances cellular transformation and tumorigenesis. Nat. Genet. 39: 673–677, 2007.
  • 24. Mateescu, B. et al. miR-141 and miR-200a act on ovarian tumorigenesis by controlling oxidative stress response. Nat. Med. 17: 1627–1635, 2011.
  • 25. Iorio, M. V. et al. microRNA signatures in human ovarian cancer. Cancer Res. 67: 8699–8707 (2007).
  • 26. Nam, E. J. et al. MicroRNA expression profiles in serous ovarian carcinoma. Clin. Cancer Res. 14: 2690–2695, 2008.
  • 27. Yang, N. et al. MicroRNA microarray identifies Let-7i as a novel biomarker anti-therapeutic target in human epithelial ovarian cancer. Cancer Res. 68: 10307–10314, 2008.
  • 28. Dahiya, N. & Morin, P. J. MicroRNAs in ovarian carcinomas. Endocr. Relat. Cancer 17: 77–89, 2010.
  • 29. Dahiya, N. et al. MicroRNA expression and identification of putative miRNA targets in ovarian cancer. PLoS One 18: e2436, 2008.
  • 30. Yu-Ming Yeh, Chi-Mu Chuang, Kuan-Chong Chao and Lu-Hai Wang. MicroRNA-138 suppresses ovarian cancer cell invasion and metastasis by targeting SOX4 and HIF-1a. Int. J. Cancer 133: 867–878, 2013.
  • 31. Lehmann S, Bykov VJ, Ali D, Andren O, Cherif H, Tidefelt U, Uggla B, Yachnin J, Juliusson G, Moshfegh A, Paul C, Wiman KG, Andersson PO. Targeting p53 in vivo: a first-in-human study with p53-targeting compound APR-246 in refractory hematologic malignancies and prostate cancer. J Clin Oncol. 30: 3633–3639, 2012.
  • 32. Livak KJ and Schmittgen TD: Analysis of relative gene expres¬sion data using real time quantitative PCR and the 2( delta delta C(T)) method. Methods 25: 402 408, 2001.
  • 33. Selivanova G, Wiman KG. Reactivation of mutant p53: molecular mechanisms and therapeutic potential. Oncogene. 2007; 26:2243–54.
  • 34. Ventura A, Kirsch DG, McLaughlin ME, Tuveson DA, Grimm J, Lintault L, Newman J, Reczek EE, Weissleder R, Jacks T. Restoration of p53 function leads to tumour regression in vivo. Nature. 2007; 445:661–5.
  • 35. Foster BA, Coffey HA, Morin MJ, Rastinejad F. Pharmacological rescue of mutant p53 conformation and function. Science. 1999; 286:2507–10.
  • 36. Bykov VJ, Issaeva N, Shilov A, Hultcrantz M, Pugacheva E, Chumakov P, Bergman J, Wiman KG, Selivanova G. Restoration of the tumor suppressor function to mutant p53 by a lowmolecular-weight compound. Nat Med. 2002; 8:282–8.
  • 37. E. Izaurralde, Gene regulation. Breakers and blockers-miRNAs at work, Science 349 (2015) 380–382.
  • 38. D.W. Thomson, M.E. Dinger, Endogenous microRNA sponges: evidence and controversy, Nat. Rev. Genet. 17 (2016) 272–283.
  • 39. Medina PP, Nolde M, Slack FJ. OncomiR addiction in an in vivo model of microRNA-21-induced pre-B-cell lymphoma. Nature. 2010; 467: 86–90.
  • 40. H. Nip, A.A. Dar, S. Saini, M. Colden, S. Varahram, H. Chowdhary, S. Yamamura, Y. Mitsui, Y. Tanaka, T. Kato, Y. Hashimoto, M. Shiina, P. Kulkarni, P. Dasgupta, M. Imai-Sumida, T.Z. Laura, K. Greene, G. Deng, R. Dahiya, M. Shahana, Oncogenic microRNA-4534 regulates PTEN pathway in prostate cancer, Oncotarget (2016).
  • 41. K. Yin, M. Liu, M. Zhang, F.Wang,M. Fen, Z. Liu, Y. Yuan, S. Gao, L. Yang,W. Zhang, J. Zhang, B. Guo, J. Xu, H. Liang, X. Chen, W. Guan, miR-208a-3p suppresses cell apoptosis by targeting PDCD4 in gastric cancer, Oncotarget (2016).
  • 42. Yamamoto, M.Mori, MicroRNAs as therapeutic targets and colorectal cancer therapeutics, Adv. Exp. Med. Biol. 937 (2016) 239–247.
  • 43. C. Han, Y. Zhou, Q. An, F. Li, D. Li, X. Zhang, Z. Yu, L. Zheng, Z. Duan, Q. Kan, MicroRNA-1 (miR-1) inhibits gastric cancer cell proliferation and migration by targeting MET, Tumour Biol. 36 (2015) 6715–6723.
  • 44. I.N. King, V. Yartseva, D. Salas, A. Kumar, A. Heidersbach, D.M. Ando, N.R. Stallings, J.L. Elliott, D. Srivastava, K.N. Ivey, The RNA-binding protein TDP-43 selectively disrupts microRNA-1/206 incorporation into the RNA-induced silencing complex, J. Biol. Chem. 289 (2014) 14263–14271.
  • 45. Cui Chang, Te Liu, Yongyi Huang, Wenxing Qin, Hongtu Yang, Juan Chen. MicroRNA-134-3p is a novel potential inhibitor of human ovarian cancer stem cells by targeting RAB27A, Gene 605 (2017) 99–107.
  • 46. Zhang YK, Wang H, Leng Y, Li ZL, Yang YF, Xiao FJ, Li QF, Chen XQ, Wang LS. Overexpression of microRNA-29b induces apoptosis of multiple myeloma cells through down regulating Mcl-1. Biochem Biophys Res Commun. 2011; 414:233–239.
  • 47. Xu L, Xu Y, Jing Z, Wang X, Zha X, Zeng C, Chen S, Yang L, Luo G, Li B, Li Y. Altered expression pattern of miR29a, miR-29b and the target genes in myeloid leukemia. Exp Hematol Oncol. 2014; 3:17.
  • 48. Manujendra N. Saha, Jahangir Abdi1, Yijun Yang1, Hong Chang. MiRNA-29a as a tumor suppressor mediates PRIMA-1Met-induced anti-myeloma activity by targeting c-Myc. Oncotarget, Vol. 7(6), 2016.
  • 49. Baohong Zhang, Xiaoping Pan, George P. Cobb, Todd A. Anderson. microRNAs as oncogenes and tumor suppressors, Developmental Biology 302 (2007) 1–12.
  • 50. Ling H, Fabbri M, Calin GA. MicroRNAs and other noncoding RNAs as targets for anticancer drug development. Nat Rev Drug Discov. 2013; 12:847–865.

ANALYSIS OF DIFFERENTIAL miRNA EXPRESSION IN RESPONSE TO PRIMA-1 Met THERAPY IN OVARIAN CANCER CELLS

Yıl 2020, , 19 - 25, 04.05.2020
https://doi.org/10.34108/eujhs.543409

Öz

Restoration of p53 function in tumor cells will be an attractive
strategy for ovarian cancer therapy since p53 mutations are found in more than
50 % of ovarian cancers. The small molecule Prima-1Met has been
shown to restore tumor suppression function of p53, inhibit cell growth and
induce apoptosis in human tumor cells. MicroRNAs (miRNAs) regulate gene
expression at both transcriptional and translational levels as well as acting in
a wide variety of physiological and biological processes. Numerous miRNAs
associated with chemotherapy resistance and disease progression have been
described in a large number of miRNA profiling studies in epithelial ovarian
cancer, but little is known about the involvement of miRNAs in response to Prima-1Met.
We aimed to determine the expression of miRNAs in response to Prima-1Met
treatment, which is known to have apoptotic effects in ovarian cancer cell
lines. The expressions of miRNAs targeting both cancer and apoptosis pathways
in drug-delivered cell lines were determined and analyzed by miScript PCR
array. As a result of the assay, the expression of miRNA-1, miRNA-134,
miRNA-141, miRNA-143, miRNA-145, miRNA-204, miRNA-205, miRNA-214, miRNA-29a and
miRNA-29c increased in response to Prima-1Met in both cell lines,
while the expression of miRNA-21, miRNA-221 and miRNA-222 was reduced. In
conclusion, this study provides a basis for elucidating the molecular mechanism
of Prima-1Met-induced apoptosis.

Kaynakça

  • 1. Sankaranarayanan R and Ferlay J: Worldwide burden of gynaecological cancer: The size of the problem. Best Pract Res Clin Obstet Gynaecol 20: 207-225, 2006.
  • 2. Levine AJ. p53, the cellular gatekeeper for growth and division. Cell 88: 323-331, 1997.
  • 3. Vogelstein B, Lane D, Levine AJ. Surfing the p53 network. Nature 408: 307-310, 2000.
  • 4. El-Hizawi S, Lagowski JP, Kulesz-Martin M, Albor A. Induction of gene amplification as a gain-offunction phenotype of mutant p53 proteins. Cancer Res 62: 3264-3270, 2002.
  • 5. Teneriello MG, Ebina M, Linnoila Rl, Henry M, Nash JD, Park RC, et al: p53 and Ki-ras gene mutations in epithelial ovarian neoplasms. Cancer Research 1993, 53:3103-8.
  • 6. Mazare R, Pujol P, Maudelonde T, Jeanteur P, Theillet C: p53 mutations in ovarian cancer: a late event? Oncogene 1991,6:1685-90.
  • 7. Eccles DM, Brett L, Lessells A, Gruber L, Lane D, Steel CM, et al: Overexpression of the p53 protein and allele loss at 17p13 in ovarian carcinoma. Br J Cancer 1992, 65:40-4.
  • 8. Kohler MF, Kerns BJ, Humphrey PA, Marks JR, Bast RC, Berchuck A: Mutation and overexpression of p53 in earlystage epithelial ovarian cancer. Obstet Gynecol 1993, 81:643-50.
  • 9. Hoe KK, Verma CS, Lane DP. Drugging the p53 pathway: understanding the route to clinical efficacy. Nat Rev Drug Discov 13: 217–36, 2014.
  • 10. Bykov VJ, Issaeva N, Shilov A, Hultcrantz M, Pugacheva E, Chumakov P, et al. Restoration of the tumor suppressor function to mutant p53 by a low molecular-weight compound. Nat Med 8: 282–8, 2002.
  • 11. Bykov VJ, Zache N, Stridh H, Westman J, Bergman J, Selivanova G, et al. PRIMA-1MET synergizes with cisplatin to induce tumor cell apoptosis. Oncogene 24: 3484–91, 2005.
  • 12. Bykov VJ, Issaeva N, Selivanova G, Wiman KG. Mutant p53-dependent growth suppression distinguishes PRIMA-1 from known anticancer drugs: a statistical analysis of information in the National Cancer Institute database. Carcinogenesis 23: 2011–8, 2002.
  • 13. Shi H, Lambert JM, Hautefeuille A, Bykov VJ, Wiman KG, Hainaut P, et al. In vitro and in vivo cytotoxic effects of PRIMA-1 on hepatocellular carcinoma cells expressing mutant p53ser249. Carcinogenesis 29: 1428–34, 2008.
  • 14. Liang Y, Besch-Williford C, Hyder SM. PRIMA-1 inhibits growth of breast cancer cells by re-activating mutant p53 protein. Int J Oncol 35: 1015–23, 2009.
  • 15. Zandi R, Selivanova G, Christensen CL, Gerds TA, Willumsen BM, Poulsen HS. PRIMA-1Met/APR-246 induces apoptosis and tumor growth delay in small cell lung cancer expressing mutant p53. Clin Cancer Res 17: 2830–41, 2011.
  • 16. Zache N, Lambert JM, Wiman KG, Bykov VJ. PRIMA-1MET inhibits growth of mouse tumors carrying mutant p53. Cell Oncol 30: 411–8, 2008.
  • 17. Liang Y, Besch-Williford C, Benakanakere I, Hyder SM. Re-activation of the p53 pathway inhibits in vivo and in vitro growth of hormone-dependent human breast cancer cells. Int J Oncol 31: 777–84, 2007.
  • 18. Synnott N, Pierce A, Mullooly M, Caiazza F, McGowan PM, O’Donovan N, et al. Mutant p53: a therapeutic target for the treatment of triple-negative breast cancer? J Clin Oncol 32(5s) [suppl; abstr 1118], 2014.
  • 19. Bartel DP. MicroRNAs: genomics, biogenesis, mechanism, function. Cell 116:281–297, 2004.
  • 20. Ambros V. The functions of animal microRNAs. Nature 431:350–355, 2004.
  • 21. Zhang B, Pan X, Cobb GP, Anderson TA. microRNAs as oncogenes and tumor suppressors. Dev Biol. 302:1–12, 2007.
  • 22. Yang, D. et al. Intregrated analyses identify a master microRNA regulatory network for the mesenchymal subtype in serous ovarian cancer. Cancer Cell 23: 186–199, 2013.
  • 23. Kumar, M. S., Lu, J., Mercer, K. L., Golub, T. R. & Jacks, T. Impaired microRNA processing enhances cellular transformation and tumorigenesis. Nat. Genet. 39: 673–677, 2007.
  • 24. Mateescu, B. et al. miR-141 and miR-200a act on ovarian tumorigenesis by controlling oxidative stress response. Nat. Med. 17: 1627–1635, 2011.
  • 25. Iorio, M. V. et al. microRNA signatures in human ovarian cancer. Cancer Res. 67: 8699–8707 (2007).
  • 26. Nam, E. J. et al. MicroRNA expression profiles in serous ovarian carcinoma. Clin. Cancer Res. 14: 2690–2695, 2008.
  • 27. Yang, N. et al. MicroRNA microarray identifies Let-7i as a novel biomarker anti-therapeutic target in human epithelial ovarian cancer. Cancer Res. 68: 10307–10314, 2008.
  • 28. Dahiya, N. & Morin, P. J. MicroRNAs in ovarian carcinomas. Endocr. Relat. Cancer 17: 77–89, 2010.
  • 29. Dahiya, N. et al. MicroRNA expression and identification of putative miRNA targets in ovarian cancer. PLoS One 18: e2436, 2008.
  • 30. Yu-Ming Yeh, Chi-Mu Chuang, Kuan-Chong Chao and Lu-Hai Wang. MicroRNA-138 suppresses ovarian cancer cell invasion and metastasis by targeting SOX4 and HIF-1a. Int. J. Cancer 133: 867–878, 2013.
  • 31. Lehmann S, Bykov VJ, Ali D, Andren O, Cherif H, Tidefelt U, Uggla B, Yachnin J, Juliusson G, Moshfegh A, Paul C, Wiman KG, Andersson PO. Targeting p53 in vivo: a first-in-human study with p53-targeting compound APR-246 in refractory hematologic malignancies and prostate cancer. J Clin Oncol. 30: 3633–3639, 2012.
  • 32. Livak KJ and Schmittgen TD: Analysis of relative gene expres¬sion data using real time quantitative PCR and the 2( delta delta C(T)) method. Methods 25: 402 408, 2001.
  • 33. Selivanova G, Wiman KG. Reactivation of mutant p53: molecular mechanisms and therapeutic potential. Oncogene. 2007; 26:2243–54.
  • 34. Ventura A, Kirsch DG, McLaughlin ME, Tuveson DA, Grimm J, Lintault L, Newman J, Reczek EE, Weissleder R, Jacks T. Restoration of p53 function leads to tumour regression in vivo. Nature. 2007; 445:661–5.
  • 35. Foster BA, Coffey HA, Morin MJ, Rastinejad F. Pharmacological rescue of mutant p53 conformation and function. Science. 1999; 286:2507–10.
  • 36. Bykov VJ, Issaeva N, Shilov A, Hultcrantz M, Pugacheva E, Chumakov P, Bergman J, Wiman KG, Selivanova G. Restoration of the tumor suppressor function to mutant p53 by a lowmolecular-weight compound. Nat Med. 2002; 8:282–8.
  • 37. E. Izaurralde, Gene regulation. Breakers and blockers-miRNAs at work, Science 349 (2015) 380–382.
  • 38. D.W. Thomson, M.E. Dinger, Endogenous microRNA sponges: evidence and controversy, Nat. Rev. Genet. 17 (2016) 272–283.
  • 39. Medina PP, Nolde M, Slack FJ. OncomiR addiction in an in vivo model of microRNA-21-induced pre-B-cell lymphoma. Nature. 2010; 467: 86–90.
  • 40. H. Nip, A.A. Dar, S. Saini, M. Colden, S. Varahram, H. Chowdhary, S. Yamamura, Y. Mitsui, Y. Tanaka, T. Kato, Y. Hashimoto, M. Shiina, P. Kulkarni, P. Dasgupta, M. Imai-Sumida, T.Z. Laura, K. Greene, G. Deng, R. Dahiya, M. Shahana, Oncogenic microRNA-4534 regulates PTEN pathway in prostate cancer, Oncotarget (2016).
  • 41. K. Yin, M. Liu, M. Zhang, F.Wang,M. Fen, Z. Liu, Y. Yuan, S. Gao, L. Yang,W. Zhang, J. Zhang, B. Guo, J. Xu, H. Liang, X. Chen, W. Guan, miR-208a-3p suppresses cell apoptosis by targeting PDCD4 in gastric cancer, Oncotarget (2016).
  • 42. Yamamoto, M.Mori, MicroRNAs as therapeutic targets and colorectal cancer therapeutics, Adv. Exp. Med. Biol. 937 (2016) 239–247.
  • 43. C. Han, Y. Zhou, Q. An, F. Li, D. Li, X. Zhang, Z. Yu, L. Zheng, Z. Duan, Q. Kan, MicroRNA-1 (miR-1) inhibits gastric cancer cell proliferation and migration by targeting MET, Tumour Biol. 36 (2015) 6715–6723.
  • 44. I.N. King, V. Yartseva, D. Salas, A. Kumar, A. Heidersbach, D.M. Ando, N.R. Stallings, J.L. Elliott, D. Srivastava, K.N. Ivey, The RNA-binding protein TDP-43 selectively disrupts microRNA-1/206 incorporation into the RNA-induced silencing complex, J. Biol. Chem. 289 (2014) 14263–14271.
  • 45. Cui Chang, Te Liu, Yongyi Huang, Wenxing Qin, Hongtu Yang, Juan Chen. MicroRNA-134-3p is a novel potential inhibitor of human ovarian cancer stem cells by targeting RAB27A, Gene 605 (2017) 99–107.
  • 46. Zhang YK, Wang H, Leng Y, Li ZL, Yang YF, Xiao FJ, Li QF, Chen XQ, Wang LS. Overexpression of microRNA-29b induces apoptosis of multiple myeloma cells through down regulating Mcl-1. Biochem Biophys Res Commun. 2011; 414:233–239.
  • 47. Xu L, Xu Y, Jing Z, Wang X, Zha X, Zeng C, Chen S, Yang L, Luo G, Li B, Li Y. Altered expression pattern of miR29a, miR-29b and the target genes in myeloid leukemia. Exp Hematol Oncol. 2014; 3:17.
  • 48. Manujendra N. Saha, Jahangir Abdi1, Yijun Yang1, Hong Chang. MiRNA-29a as a tumor suppressor mediates PRIMA-1Met-induced anti-myeloma activity by targeting c-Myc. Oncotarget, Vol. 7(6), 2016.
  • 49. Baohong Zhang, Xiaoping Pan, George P. Cobb, Todd A. Anderson. microRNAs as oncogenes and tumor suppressors, Developmental Biology 302 (2007) 1–12.
  • 50. Ling H, Fabbri M, Calin GA. MicroRNAs and other noncoding RNAs as targets for anticancer drug development. Nat Rev Drug Discov. 2013; 12:847–865.
Toplam 50 adet kaynakça vardır.

Ayrıntılar

Birincil Dil Türkçe
Konular Klinik Tıp Bilimleri
Bölüm Araştırma Makalesi
Yazarlar

Nilüfer İmir

Esra Aydemir

Ece Şimşek

Yayımlanma Tarihi 4 Mayıs 2020
Gönderilme Tarihi 22 Mart 2019
Yayımlandığı Sayı Yıl 2020

Kaynak Göster

APA İmir, N., Aydemir, E., & Şimşek, E. (2020). OVER KANSERİ HÜCRELERİNDE PRİMA-1 Met TEDAVİSİNE YANIT OLARAK DEĞİŞEN miRNA EKSPRESYON ANALİZİ. Sağlık Bilimleri Dergisi, 29(1), 19-25. https://doi.org/10.34108/eujhs.543409
AMA İmir N, Aydemir E, Şimşek E. OVER KANSERİ HÜCRELERİNDE PRİMA-1 Met TEDAVİSİNE YANIT OLARAK DEĞİŞEN miRNA EKSPRESYON ANALİZİ. JHS. Mayıs 2020;29(1):19-25. doi:10.34108/eujhs.543409
Chicago İmir, Nilüfer, Esra Aydemir, ve Ece Şimşek. “OVER KANSERİ HÜCRELERİNDE PRİMA-1 Met TEDAVİSİNE YANIT OLARAK DEĞİŞEN MiRNA EKSPRESYON ANALİZİ”. Sağlık Bilimleri Dergisi 29, sy. 1 (Mayıs 2020): 19-25. https://doi.org/10.34108/eujhs.543409.
EndNote İmir N, Aydemir E, Şimşek E (01 Mayıs 2020) OVER KANSERİ HÜCRELERİNDE PRİMA-1 Met TEDAVİSİNE YANIT OLARAK DEĞİŞEN miRNA EKSPRESYON ANALİZİ. Sağlık Bilimleri Dergisi 29 1 19–25.
IEEE N. İmir, E. Aydemir, ve E. Şimşek, “OVER KANSERİ HÜCRELERİNDE PRİMA-1 Met TEDAVİSİNE YANIT OLARAK DEĞİŞEN miRNA EKSPRESYON ANALİZİ”, JHS, c. 29, sy. 1, ss. 19–25, 2020, doi: 10.34108/eujhs.543409.
ISNAD İmir, Nilüfer vd. “OVER KANSERİ HÜCRELERİNDE PRİMA-1 Met TEDAVİSİNE YANIT OLARAK DEĞİŞEN MiRNA EKSPRESYON ANALİZİ”. Sağlık Bilimleri Dergisi 29/1 (Mayıs 2020), 19-25. https://doi.org/10.34108/eujhs.543409.
JAMA İmir N, Aydemir E, Şimşek E. OVER KANSERİ HÜCRELERİNDE PRİMA-1 Met TEDAVİSİNE YANIT OLARAK DEĞİŞEN miRNA EKSPRESYON ANALİZİ. JHS. 2020;29:19–25.
MLA İmir, Nilüfer vd. “OVER KANSERİ HÜCRELERİNDE PRİMA-1 Met TEDAVİSİNE YANIT OLARAK DEĞİŞEN MiRNA EKSPRESYON ANALİZİ”. Sağlık Bilimleri Dergisi, c. 29, sy. 1, 2020, ss. 19-25, doi:10.34108/eujhs.543409.
Vancouver İmir N, Aydemir E, Şimşek E. OVER KANSERİ HÜCRELERİNDE PRİMA-1 Met TEDAVİSİNE YANIT OLARAK DEĞİŞEN miRNA EKSPRESYON ANALİZİ. JHS. 2020;29(1):19-25.