Mini Review Open Access
Pathological Function and Clinical Significance of Microrna- 10b in Cancer
Ya-Ching Lu and Ann-Joy Cheng*
1Department of Medical Biotechnology, College of Medicine, Chang Gung University, 259 Wen-Hwa 1st Road, Taoyuan 333, Taiwan

*Corresponding author: Ann-Joy Cheng, Professor, Department of Medical Biotechnology, College of Medicine, Chang Gung University, 259 Wen-Hwa 1st Road, Taoyuan 333, Taiwan, Tel: 886-3-211-88080; ex: 5085; Fax: 886-3-211-8247; E-mail: @
Received: March 05, 2014 ; Accepted: April 10, 2014; Published: April 14, 2014
Citation: Lu YC, Cheng AJ (2014) Pathological Function and Clinical Significance of Microrna-10b in Cancer. Cancer Sci Res Open Access 1(2): 1-5.
Abstract Top
Micro RNAs, the endogenous non-coding small RNAs are found involved in cancer pathogenesis. Identification of the miRNA signature in cancer and understanding the underlined regulatory mechanism provide information for clinical decision. Increasing evidences show that miR-10b plays important role in cancer progression and metastasis, thus it may be a therapeutic target for cancer control. Moreover, the alternations of miR-10b expression in malignant diseases provide great potential to use this molecule as a cancer biomarker for early detection, disease assessment or therapeutic monitoring. In this article, we review current knowledge about the cellular function of miR-10b, and discuss its clinical significance and potential application in cancer.
Keywords: microRNA-10b; Clinical significance; Cancer
miRNA Discovery, Biogenesis, Action Mechanism and DetectionTop
MicroRNAs (miRNAs) are small, non-coding RNA molecules encoded in the genomes, with length in range of 18-25 nucleotides. These molecules are transcribed from hairpin-loop primary ribonucleotides (pri-miRNA) by RNA polymerase II [1,2]. Pri-miRNAs are processed by RNase-III family enzyme, Dorsha, and then become 70nt precursor miRNA (pre-miRNA). The pre-miRNA is exported out to the cytoplasm by Exportin-5, in a Ran-GTP-dependent manner. In the cytoplasm, the pre-miRNA is cleaved by Dicer to generate a 20-bp duplex intermediate [2,3], and further unwound to mature miRNA. In order to control target gene expression, the single strand mature miRNA must associate with the RNA-induced silencing complex (RISC) [4]. Once miRNA incorporates into RISC, the miRNA guides the complex to its target by base-pairing with the target mRNA.

The first identified miRNA is lin-4, which has been discovered in Caenorhabditis elegans [5]. This 22 nucleotide small RNA is shown to interact with the 3′ un-translated region (3′-UTR) of the lin-14 mRNA and to repress its expression [6,7]. It is now clear that miRNAs regulate their targets by inhibition of protein synthesis or by direct cleavage of the target mRNA, according to the degree of complementarities with their targets 3′-UTR region. When miRNA is perfectly complementary binding, the target mRNA will be degraded, whereas when partial complementary binding, target protein translation will be blocked [8]. In the past decade, novel miRNA molecules were discovered across in many sapiens. Till now, there are 1872 precursors, and 2578 mature miRNAs sequence in Homo sapiens listed in miRBase (release 20). Through miRNA target predictions, it is estimated that up to 30% of the genes are under control by currently known miRNAs in mammals [9,10]. Each mammalian miRNA regulates ~200 target genes in average through interaction with the seed sequences of the complementary target sites [9,11]. All of these findings suggest that miRNA has become a big family of gene regulators. Furthermore, detection of mature miRNAs is another challenge because of small size and the sequence similarity among various members. Before, northern blot was considered a gold standard for miRNA detection. However, time consuming and less sensitivity of this assay was shown [12]. Several approaches are improved for miRNAs detection, including quantitative reverse transcription PCR (RT-PCR), hybridization-based method and next generation sequencing [13]. The detection method improvement contributes to accomplish miRNA studies in disease and in clinical application.
The Physiological Functions of miRNAs in CancerTop
Accumulating studies have strongly supported the roles of miRNAs regulating in various crucial cellular processes, including cell proliferation [14], apoptosis [15], development [16], differentiation [17] and metabolism [9]. In addition, miRNAs alteration through disrupting the homeostasis of biological process often leads to many human diseases, such as cancer [10,18,19]. There are 50% miRNA genes identified localized in cancer associated genomics region (CAGR) or fragile sites suggesting the correlation between miRNA and cancer disease [11]. Evidences demonstrated that miRNAs could act as oncogenes or tumor suppressive genes to participate in tumorigenesis [20,21]. Over-expression of a miRNA that targets to a specific tumor suppressive gene could result in loss of the molecular protective factor. In contrast, less expression of a miRNA targeting to a specific proto-oncogene could lead to excessive amount of the oncogenic protein expression [22-24]. Besides, increasing reports reveal that miRNAs through regulating Accumulating studies have strongly supported the roles of miRNAs regulating in various crucial cellular processes, including cell proliferation [14], apoptosis [15], development [16], differentiation [17] and metabolism [9]. In addition, miRNAs alteration through disrupting the homeostasis of biological process often leads to many human diseases, such as cancer [10,18,19]. There are 50% miRNA genes identified localized in cancer associated genomics region (CAGR) or fragile sites suggesting the correlation between miRNA and cancer disease [11]. Evidences demonstrated that miRNAs could act as oncogenes or tumor suppressive genes to participate in tumorigenesis [20,21]. Over-expression of a miRNA that targets to a specific tumor suppressive gene could result in loss of the molecular protective factor. In contrast, less expression of a miRNA targeting to a specific proto-oncogene could lead to excessive amount of the oncogenic protein expression [22-24]. Besides, increasing reports reveal that miRNAs through regulating
Role of microRNA-10b in Cancers and the Molecular Regulatory MechanismTop
The miR-10b is located on human chromosome 2q31, between Hoxd4 and Hoxd8 genes in genome sequence [50]. In 2005, miR-10b was first discovered associated with cancer, by over-expression in glioblastoma cells through microarray analysis [51]. At the same year, through comparing microRNA profiling between cancer and normal tissue samples, this miRNA was also found altered expression in breast cancer. The potential targets were identified, as FLT1, BDNF and SHC1 [52]. The report of miR-10b by Ma et al. [39] further draws attention. They found that miR-10b was highly expressed in metastatic cancer cells than either primary human mammary epithelial cells (HMECs) or spontaneously immortalized MCF-10A cells [39]. In accord with the expression pattern in cultured cells, breast carcinoma tumor cells obtained from metastasis-free patients showed lower level of miR-10b expression [52]. In contrast, miR-10b was elevated in primary tumors obtained from metastasispositive patients [39,52] concluded that miR-10b participates in the metastatic process rather than the tumor initiating stage during the development of breast cancer [39]. Thereafter, many molecular findings further supported the significance of miR-10b in cancer. It was found that miR-10b inhibited the synthesis of HOXD10 which facilitated the expression of prometastatic genes (RhoA/RhoC, urokinase plasminogen activator receptor, α3-integrin, and MT1-MMP), leading to cell migration and invasion in breast cancer [39,41,53]. Similarly, miR-10b down-regulated syndecan-1, which induced the expressions of transcription factors (AML1/RUNX1 and ATF2), resulting to cellcycle progression and metastasis [54]. Furthermore, miR-10b may modulate metastasis in breast cancer through E-cadherin associated mechanism or TGF-induced epithelial-mesenchymal transition [55,56]. Aside from breast cancer, miR-10b also participates in the progression of other malignant diseases Inhibition of miR-10b through inducing neurofibromin and RAS signaling resulted in the suppressions of cell proliferation, migration and invasion in neurofibromatosis type 1 malignant peripheral nerve sheath tumors (MPNSTs) [57]. In gastric cancer, miR-10b through targeting to HOXD10 stimulated RhoC and AKT phosphorylation to promote cell invasion [47]. In pancreatic cancer, miR-10b enhanced EGFR phosphorylation, ER1/2 activation, and EGF-induced cell invasion through targeting to Tat-interactin protein 30 (TIP30) [46]. In nasopharyngeal cancer, latent membrane protein-1 in Epstein-Barr virus induced twist activation, resulting to up-regulation of miR-10b expression to enhance cancer metastasis [58]. In bladder cancer, the regulatory mechanisms of miR-10b/KLF4/E-cadherin and miR-10b/HOXD10/MMP14 were found to promote cell invasion [44]. In head-neck cancer, miR-10b facilitated cell migration and invasion, while minimal effects on cell growth or stress response [48]. Most studies revealed that miR-10b participated in metastasis regulation. Nevertheless, it was also found involved in glioma cell growth and cell death [49]. In glioblatoma, miR-10b regulated cell proliferation and apoptosis by targeting to cell cycle inhibitor (BCL2L11/Bim) and proapoptotic genes (TFAP2C/ AP-2g, CDKN1A/p21, and CDKN2A/p16) [59]. Collectively, miR- 10b plays oncogenic function in common cancers. However, the molecular mechanisms may be very dependent on specific tissue type.
Clinical Significance and Potential Applications of miR-10b in CancerTop
Therapeutic application of miRNA may be used by two ways: miRNA antagonists and miRNA mimics. Treatments of miRNA antagonist or miRNA mimic may lead to gain- or lossof the specific miRNA in the diseased tissues. Recent works showed that miRNA mimics have been developed in the stage of the preclinical trial for solid tumor treatment. For example, therapeutic delivery of let-7 mimic which targets to oncogene RAS led to a robust inhibition of tumor growth in xenografted mouse or KRAS-G12S transgenic mouse [60]. Another approach by targeting of metastatic- suppressive miRNAs could serve as a novel strategy to inhibit cancer spread. Since miR-10b plays a crucial role in regulating metastatic behavior, investigators intend to develop agents directly against this molecule. It has shown that systemic treatment of miR-10b antagonist to tumor-bearing mice markedly suppressed the formation of lung metastatic nodules [61]. Another design by a nanodrug, which features a nanoparticle with RGD (tripeptide arginine-glycine-aspartic acid) decorated with locked nucleic acid oligonucleotides also showed a therapeutic ability. This anti-miR-10b nanodrug prevented the metastasis process in orthotopic tumor bearing mice [62].
The emergence of miRNAs as mediators of gene regulation suggesting these molecules could serve as biomarkers for diagnosis or prognosis. It has shown that miR-10b expression determined by in situ hybridization is highly correlated with cancer occurrence, therapy response, and prognosis in pancreatic ductal adenocarcinoma [63,64]. Recently, circulating miRNAs, which can be detected in the body fluids, as in saliva, urine and plasma, are thought to serve as minimally invasive biomarkers [65, 66]. MiR-10b has been reported possessing high potential of cancer marker. For example, the circulating levels of miR-10b, miR-34a and miR-155 correlated with the metastatic status in breast cancer [67]. Another report showed that the combination of circulating miR-10b and miR-373 helps to assess lymph node status of breast cancer [68]. Similarly, serum miR-10b was also reported over-expressed in the breast cancer patients with bone metastasis [69]. Collectively, miR-10b may be used as biomarker to monitor metastatic status of breast cancer. Furthermore, the increasing level of miR-10b was also found in colorectal cancer with higher staged, indicating the potential of this molecule as a biomarker for aggressive malignant disease [70]. Nevertheless, another association of miR-10b was also reported in other cancer types. In esophageal carcinoma, the elevated expression of miR-10b was found in 95% of the cancer tissues compared to the normal counterparts, while without clinical correlation with metastatic status [45]. Similarly, up-regulation of miR-10b in plasma was found in approximately 90% of the patients with oral cancer, and serving high discriminative power with normal subjects (AUC=0.932). Furthermore, this elevation of miR-10b was also significantly higher in the plasma of patient with oral precancer lesions, suggesting the potential use of miR-10b as an early detection marker for oral cancer [48].
ConclusionsTop
Through understanding of the mechanism of miR-10b in pathological function provides the novel strategy for clinical applications. Increasing evidences have demonstrated the important role of miR-10b during cancer progression, especially on metastasis. Using miR-10b antagomir to regulate multiple down-stream target genes may serve an effective therapeutic approach. Furthermore, the association between miR-10b expression and clinical pathological status suggest the potential use of this molecule as biomarker in various cancers. To better detection of miR-10b alteration in body fluids should provide minimal invasive tool for cancer diagnosis, disease assessment, or therapeutic monitoring. In summary, miR-10b plays an important role in cancer progression, and significantly different in different status of diseases. Summarizing the carcinogenic significance of miR-10b would further lead to translation impacts of applying this molecule in cancer management.
ReferencesTop
  1. Kim VN (2005) MicroRNA biogenesis: coordinated cropping and dicing. Nat Rev Mol Cell Biol 6(5): 376-385.
  2. Pillai RS (2005) MicroRNA function: multiple mechanisms for a tiny RNA? RNA 11(12): 1753-1761
  3. Lee Y, Jeon K, Lee JT, Kim S, Kim VN (2002) MicroRNA maturation: stepwise processing and subcellular localization. Embo J 21(17): 4663-4670.
  4. Schwarz DS, Hutvagner G, Du T, Xu Z, Aronin N, et al. (2003) Asymmetry in the assembly of the RNAi enzyme complex. Cell 115(2): 199-208.
  5. Wightman B, I. Ha, G. Ruvkun (1993) Posttranscriptional regulation of the heterochronic gene lin-14 by lin-4 mediates temporal pattern formation in C. elegans. Cell 75(5): 855-862
  6. Lee R C, RL Feinbaum, V Ambros (1993) The C. elegans heterochronic gene lin-4 encodes small RNAs with antisense complementarity to lin- 14. Cell 75(5): 843-854.
  7. Olsen PH, Ambros V (1999) The lin-4 regulatory RNA controls developmental timing in Caenorhabditis elegans by blocking LIN-14 protein synthesis after the initiation of translation. Dev Biol 216(2): 671-680.
  8. Bartel DP (2004) MicroRNAs: genomics, biogenesis, mechanism, and function. Cell 116(2): 281-297.
  9. Roldo C, Missiaglia E, Hagan JP, Falconi M, Capelli P, et al. (2006) MicroRNA expression abnormalities in pancreatic endocrine and acinar tumors are associated with distinctive pathologic features and clinical behavior. J Clin Oncol 24(29): 4677-4684.
  10. Garzon R, Fabbri M, Cimmino A, Calin GA, Croce CM (2006) et al., MicroRNA expression and function in cancer. Trends Mol Med 12(12): 580-587.
  11. Calin GA, Sevignani C, Dumitru CD, Hyslop T, Noch E, et al. (2004) Human microRNA genes are frequently located at fragile sites and genomic regions involved in cancers. Proc Natl Acad Sci U S A 101(9): 2999-3004.
  12. Cissell KA, Deo SK (2009) Trends in microRNA detection. Anal Bioanal Chem 394(4): 1109-1116.
  13. de Planell-Saguer M, Rodicio MC (2013) Detection methods for microRNAs in clinic practice. Clin Biochem 46(10-11): 869-878.
  14. Cheng AM, Byrom MW, Shelton J, Ford LP (2005) Antisense inhibition of human miRNAs and indications for an involvement of miRNA in cell growth and apoptosis. Nucleic Acids Res 33(4): 1290-1297.
  15. Jovanovic M, Hengartner MO (2006) miRNAs and apoptosis: RNAs to die for. Oncogene 25(46): 6176-6187.
  16. Wienholds E, Plasterk RH (2005) MicroRNA function in animal development. FEBS Lett 579(26): 5911-5922.
  17. Chen CZ1, Li L, Lodish HF, Bartel DP (2004) MicroRNAs modulate hematopoietic lineage differentiation. Science 303(5654): 83-86.
  18. Zhang W, Dahlberg JE, Tam W (2007) MicroRNAs in tumorigenesis: a primer. Am J Pathol 171(3): 728-738.
  19. Calin GA, Croce CM (2006) MicroRNA signatures in human cancers. Nat Rev Cancer 6(11): 857-866.
  20. Zhang B, Pan X, Cobb GP, Anderson TA (2007) microRNAs as oncogenes and tumor suppressors. Dev Biol 302(1): 1-12.
  21. Ahmad J, Hasnain SE, Siddiqui MA, Ahamed M, Musarrat J, et al. (2013) MicroRNA in carcinogenesis & cancer diagnostics: a new paradigm. Indian J Med Res 137(4): 680-694.
  22. Li M1, Li J, Ding X, He M, Cheng SY (2010) microRNA and cancer. AAPS J 12(3): 309-317.
  23. Yu SL, Chen HY, Yang PC, Chen JJ (2007) Unique MicroRNA signature and clinical outcome of cancers. DNA Cell Biol 26(5): 283-292.
  24. Negrini M, Ferracin M, Sabbioni S, Croce CM (2007) MicroRNAs in human cancer: from research to therapy. J Cell Sci 120(11): 1833- 1840.
  25. Cheng Q, Yi B, Wang A, Jiang X (2013) Exploring and exploiting the fundamental role of microRNAs in tumor pathogenesis. Onco Targets Ther 6: 1675-1684.
  26. Calin GA, Dumitru CD, Shimizu M, Bichi R, Zupo S, et al. (2002) Frequent deletions and down-regulation of micro- RNA genes miR15 and miR16 at 13q14 in chronic lymphocytic leukemia. Proc Natl Acad Sci U S A, 99(24): 15524-15529.
  27. Cimmino A, Calin GA, Fabbri M, Iorio MV, Ferracin M, et al. (2005) miR-15 and miR-16 induce apoptosis by targeting BCL2. Proc Natl Acad Sci USA 102(39): 13944-13949.
  28. Bonci D, Coppola V, Musumeci M, Addario A, Giuffrida R, et al. (2008) The miR-15a-miR-16-1 cluster controls prostate cancer by targeting multiple oncogenic activities. Nat Med 14(11): 1271-1277.
  29. Xia L, Zhang D, Du R, Pan Y, Zhao L, et al. (2008) miR-15b and miR- 16 modulate multidrug resistance by targeting BCL2 in human gastric cancer cells. International journal of cancer. Int J Cancer 123(2): 372- 379.
  30. Frankel LB, Christoffersen NR, Jacobsen A, Lindow M, Krogh A, et al. (2008) Programmed cell death 4 (PDCD4) is an important functional target of the microRNA miR-21 in breast cancer cells. J Biol Chem 283(2): 1026-1033.
  31. Zhu S, Wu H, Wu F, Nie D, Sheng S, et al. (2008) MicroRNA-21 targets tumor suppressor genes in invasion and metastasis. Cell Res 18(3): 350-359.
  32. Meng F, Henson R, Wehbe-Janek H, Ghoshal K, Jacob ST, et al. (2007) MicroRNA-21 regulates expression of the PTEN tumor suppressor gene in human hepatocellular cancer. Gastroenterology 133(2): 647- 58.
  33. Zhu S, Si ML, Wu H, Mo YY (2007) MicroRNA-21 targets the tumor suppressor gene tropomyosin 1 (TPM1). J Biol Chem 282(19): 14328- 14336.
  34. Zhang Z, Li Z, Gao C, Chen P, Chen J, et al. (2008) miR-21 plays a pivotal role in gastric cancer pathogenesis and progression. Lab Invest 88(12): 1358-1366.
  35. Asangani IA, Rasheed SA, Nikolova DA, Leupold JH, Colburn NH, et al. (2008) MicroRNA-21 (miR-21) post-transcriptionally downregulates tumor suppressor Pdcd4 and stimulates invasion, intravasation and metastasis in colorectal cancer. Oncogene 27(15): 2128-2136.
  36. Yan LX, Huang XF, Shao Q, Huang MY, Deng L, et al. (2008) MicroRNA miR-21 overexpression in human breast cancer is associated with advanced clinical stage, lymph node metastasis and patient poor prognosis. RNA 14(11): 2348-2360.
  37. Zhang JG, Wang JJ, Zhao F, Liu Q, Jiang K, et al. (2010) MicroRNA-21 (miR-21) represses tumor suppressor PTEN and promotes growth and invasion in non-small cell lung cancer (NSCLC). Clin Chim Acta 411(11-12): 846-852.
  38. Li T, Li D, Sha J, Sun P, Huang Y (2009) MicroRNA-21 directly targets MARCKS and promotes apoptosis resistance and invasion in prostate cancer cells. Biochem Biophys Res Commun 383(3): 280-285.
  39. Ma L, Teruya-Feldstein J, Weinberg RA (2007) Tumour invasion and metastasis initiated by microRNA-10b in breast cancer. Nature 449(7163): 682-688.
  40. Gee HE, Camps C, Buffa FM, Colella S, Sheldon H, et al. (2008) MicroRNA-10b and breast cancer metastasis. Nature 455(7216).
  41. Ma L (2010) Role of miR-10b in breast cancer metastasis. Breast cancer Res 12(5): 210.
  42. Moriarty CH1, Pursell B, Mercurio AM (2010) miR-10b targets Tiam1: implications for Rac activation and carcinoma migration. J Biol Chem 285(27): 20541-20546.
  43. Nakayama I, Shibazaki M, Yashima-Abo A, Miura F, Sugiyama T, et al. (2013) Loss of HOXD10 expression induced by upregulation of miR-10b accelerates the migration and invasion activities of ovarian cancer cells. International journal of oncology 43(1): 63-71.
  44. Xiao H, Li H, Yu G, Xiao W, Hu J, et al. (2014) MicroRNA-10b promotes migration and invasion through KLF4 and HOXD10 in human bladder cancer. Oncol Rep 31(4): 1832-1838.
  45. Tian Y, Luo A, Cai Y, Su Q, Ding F, et al. (2010) MicroRNA-10b promotes migration and invasion through KLF4 in human esophageal cancer cell lines. J Biol Chem 285(11): 7986-7994.
  46. Ouyang H, Gore J, Deitz S, Korc (2013) MmicroRNA-10b enhances pancreatic cancer cell invasion by suppressing TIP30 expression and promoting EGF and TGF-beta actions. Oncogene.
  47. Liu Z, Zhu J, Cao H, Ren H, Fang X (2012) miR-10b promotes cell invasion through RhoC-AKT signaling pathway by targeting HOXD10 in gastric cancer. Int J Oncol 40(5): 1553-1560.
  48. Lu YC, Chen YJ, Wang HM, Tsai CY, Chen WH, et al. (2012) Oncogenic function and early detection potential of miRNA-10b in oral cancer as identified by microRNA profiling. Cancer Prev Res 5(4): 665-674.
  49. Gabriely G, Yi M, Narayan RS, Niers JM, Wurdinger T, et al. (2011) Human glioma growth is controlled by microRNA-10b. Cancer Res 71(10): 3563-3572.
  50. Lagos-Quintana M, Rauhut R, Meyer J, Borkhardt A, Tuschl T (2003) New microRNAs from mouse and human. Rna 9(2): 175-179.
  51. Ciafrè SA, Galardi S, Mangiola A, Ferracin M, Liu CG, et al. (2005) Extensive modulation of a set of microRNAs in primary glioblastoma. Biochem Biophys Res Commun 334(4): 1351-1358.
  52. Iorio MV, Ferracin M, Liu CG, Veronese A, Spizzo R, et al. (2005) MicroRNA gene expression deregulation in human breast cancer. Cancer Res 65(16): 7065-7070.
  53. Bourguignon LY, Wong G, Earle C, Krueger K, Spevak CC (2010) Hyaluronan-CD44 interaction promotes c-Src-mediated twist signaling, microRNA-10b expression, and RhoA/RhoC up-regulation, leading to Rho-kinase-associated cytoskeleton activation and breast tumor cell invasion. J Biol Chem 285(47): 36721-36735.
  54. Ibrahim SA, Yip GW, Stock C, Pan JW, Neubauer C, et al. (2012) Targeting of syndecan-1 by microRNA miR-10b promotes breast cancer cell motility and invasiveness via a Rho-GTPase- and E-cadherin-dependent mechanism. Int J Cancer 131(6): 884-896.
  55. Liu Y, Zhao J, Zhang PY, Zhang Y, Sun SY, et al. (2012) MicroRNA-10b targets E-cadherin and modulates breast cancer metastasis. Med Sci Monit 18(8): 299-308.
  56. Han X, Yan S, Weijie Z, Feng W, Liuxing W, et al. (2014) Critical role of miR-10b in transforming growth factor-beta1-induced epithelialmesenchymal transition in breast cancer. Cancer Gene Ther 21(2): 60-67.
  57. Chai G, Liu N, Ma J, Li H, Oblinger JL, et al. (2010) MicroRNA-10b regulates tumorigenesis in neurofibromatosis type 1. Cancer science 101(9): 1997-2004.
  58. Li G, Wu Z, Peng Y, Liu X, Lu J, et al. (2010) MicroRNA-10b induced by Epstein-Barr virus-encoded latent membrane protein-1 promotes the metastasis of human nasopharyngeal carcinoma cells. Cancer Lett 299(1): 29-36.
  59. Gabriely G, Teplyuk NM, Krichevsky AM (2011) Context effect: microRNA-10b in cancer cell proliferation, spread and death. Autophagy 7(11): 1384-1386.
  60. Trang P, Medina PP, Wiggins JF, Ruffino L, Kelnar K, et al. (2010) Regression of murine lung tumors by the let-7 microRNA. Oncogene 29(11): 1580-1587.
  61. Ma L, Reinhardt F, Pan E, Soutschek J, Bhat B, et al. (2010) Therapeutic silencing of miR-10b inhibits metastasis in a mouse mammary tumor model. Nat Biotechnol 28(4): 341-347.
  62. Yigit MV, Ghosh SK, Kumar M, Petkova V, Kavishwar A, et al. (2013) Context-dependent differences in miR-10b breast oncogenesis can be targeted for the prevention and arrest of lymph node metastasis. Oncogene 32(12): 1530-1538.
  63. Setoyama T, Zhang X, Natsugoe S, Calin GA (2011) microRNA-10b: a new marker or the marker of pancreatic ductal adenocarcinoma? Clin cancer Res 17(17): 5527-5529.
  64. Preis M, Gardner TB, Gordon SR, Pipas JM, Mackenzie TA, et al. (2011) MicroRNA-10b expression correlates with response to neoadjuvant therapy and survival in pancreatic ductal adenocarcinoma. Clin Cancer Res 17(17): 5812-5821.
  65. Kosaka N, Iguchi H, Ochiya T (2010) Circulating microRNA in body fluid: a new potential biomarker for cancer diagnosis and prognosis. Cancer Sci 101(10): 2087-2092.
  66. Bartels CL, Tsongalis GJ (2009) MicroRNAs: novel biomarkers for human cancer. Clin chem 55(4): 623-631.
  67. Roth C, Rack B, Müller V, Janni W, Pantel K, et al. ( 2010) Circulating microRNAs as blood-based markers for patients with primary and metastatic breast cancer. Breast cancer Res 12(6): R90.
  68. Chen W, Cai F, Zhang B, Barekati Z, Zhong XY (2013) The level of circulating miRNA-10b and miRNA-373 in detecting lymph node metastasis of breast cancer: potential biomarkers. Tumour Biol 34(1): 455-462.
  69. Zhao FL, Hu GD, Wang XF, Zhang XH, Zhang YK, et al. (2012) Serum overexpression of microRNA-10b in patients with bone metastatic primary breast cancer. J Int Med Res 40(3): 859-866.
  70. Chang KH, Miller N, Kheirelseid EA, Lemetre C, Ball GR, et al. (2011) MicroRNA signature analysis in colorectal cancer: identification of expression profiles in stage II tumors associated with aggressive disease. Int J Colorectal Dis 26(11): 1415-1422.
 
Listing : ICMJE   

Creative Commons License Open Access by Symbiosis is licensed under a Creative Commons Attribution 3.0 Unported License