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Granulosa cells (GCs) are essential somatic cells in the ovaries, and apoptosis of GCs causes follicular atresia. microRNA-10b (miR-10b) is pivotal for cell apoptosis. However, currently, little is known about the role of miR-10b in bovine ovarian GCs (BGCs). In this study, the effect of miR-10b on the apoptosis of BGCs was investigated. Our results showed that the overexpression of miR-10b could increase the apoptosis rate of BGCs, which is associated with the increased expression of Caspase-3 and decreased expression ratio of Bcl-2/Bax (P 0.05). Furthermore, plasminogen activator inhibitor-1 (PAI-1) was confirmed to be a validated target of miR-10b in BGCs using dual-luciferase reporter analysis, and transfection of miR-10b mimics decreased the expression of PAI-1 (P 0.05). In addition, overexpression of PAI-1 significantly inhibited BGC apoptosis (P 0.05), and PAI-1 could alleviate BGC apoptosis induced by miR-10b (P 0.05). Subsequently, phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) was found to be the downstream pathway of PAI-1 by RNA-Seq analysis and verified by Western blot. Finally, a PI3K/AKT inhibitor (Miltefosine) was used to inhibit the PI3K/AKT pathway, which reversed the inhibitory effect of PAI-1 on the apoptosis of BGCs (P 0.05), and enhanced the promotion effect of miR-10b on the apoptosis of BGCs (P 0.05). Our results indicated that miR-10b promotes BGC apoptosis by targeting PAI-1 to regulate the PI3K/AKT pathway.

It is believed that microRNAs (miRNAs) participate in the pathogenesis of Alzheimer's disease (AD), but the specified function of miR-10b-5p in the disease has not been thoroughly understood. Thereafter, this research aimed to assess the function of miR-10b-5p in AD.Rat AD models were established by injected with amyloid-βMiR-10b-5p was upregulated while HOXD10 was downregulated, and the Rho/ROCK signalling pathway was activated in hippocampal tissues of rats with AD. Inhibition of miR-10b-5p could attenuate the neuronal apoptosis, pathological injury, inflammation reaction, and oxidative stress by elevating HOXD10 and inhibiting the Rho/ROCK signalling pathway in AD rats. Moreover, HOXD10 was targeted by miR-10b-5p.Inhibited miR-10b-5p decelerated the development of AD by promoting HOXD10 and inactivating the Rho/ROCK signalling pathway, and our findings may contribute to the exploration of AD treatment.

Background and aims Among the factors associated with cancer are the oxidative stress and increased expression of some microRNA (miRs). Silibinin has an anti-tumor effect. Therefore, this study evaluates the effects of silibinin on oxidative stress indices and miR-10b expression in the animal models of breast cancer. Material and methods In this study, 48 Balb/c mice were divided into six groups (each group contains eight mice): the healthy control, the cancer control, the healthy group receiving 20 mg of silibinin, the cancer group receiving 20 mg of silibinin, the cancer group receiving 40 mg of silibinin and the cancer group receiving 80 mg of silibinin for three weeks. In order to induce cancer, 4T1 cell line was used. After obtaining breast tumor samples, the levels of Malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPX) and miR-10b expression in breast tumor biopsy were evaluated. Data were analyzed using one-way ANOVA, Kruskal–Wallis, Mann–Whitney and t-test (p Results The use of silibinin at different doses increased the activity of SOD and GPX (significantly) and the level of TAC (significantly) in the treatment group compared to untreated cancerous mice, but mir-10b and MDA were decreased non-significant and significantly respectively. Conclusion Silibinin led to a non-significant reduction of miR-10b in the treatment group compared to untreated cancerous mice. Silibinin has been shown to improve oxidative stress in breast cancer mice.

Herein, we develop a fluorescent sensor for simple detection of miRNA-10b, which combines the fluorescence quenching ability of graphene oxide (GO) and the duplex-specific nuclease (DSN) mediated target recycling amplification. Our sensor exhibits desirable sensitivity for miRNA-10b with a 530 fM detection limit that could be achieved within 75 min. Furthermore, our sensor showed good selectivity for discriminating target miRNA and other microRNAs.

We conducted a study to evaluate the prognostic and diagnostic values of microRNA-10b (miR-10b) in gastric cancer (GC) based on meta-analysis and TCGA database. Relevant studies were searched in English and Chinese database and meta-analysis was conducted on Stata 12.0. The expression value of miR-10b and clinical parameters of GC patients were downloaded from TCGA database, and relevant analyses were conducted on SPSS. High expression of miR-10b was linked with unfavorable overall survival (OS) in GC (HR = 1.572, 95% CI: 1.240–1.992, P

Background: Melanoma is one of the most invasive cutaneous cancers with characteristics such as rapid progression and distant metastasis. The early diagnosis and staging of melanoma can help better manage the patients. The current study is aimed to assess the values of microRNA-10b (miRNA-10b) in the discrimination of metastatic melanomas. Materials and Methods: The current cross-sectional study has been conducted on forty patients diagnosed with melanoma since 2011. Cell culture of melanoma cell lines derived from the cancerous tissue, including WM115, BLM, K1735, WM793, and A375M, was cultured. In order to assess miRNA-10b levels, the real-time polymerase chain reaction was utilized. The absence (n = 20)/presence (n = 20) of metastasis was diagnosed with chest computed tomography or chest X-ray. The values of miRNA-10b for the discrimination of metastasis incidence were assessed. Results: The demographic characteristics, including age and gender of the metastatic and nonmetastatic patients, were similar (P > 0.05). The specimen cultures were positive for miRNA-10b in 14 (35%) of the metastatic cases versus 4 (20%) of the nonmetastatic ones (P = 0.004). The quantitative analysis of miR-2b revealed significantly higher levels in metastatic cases (−1.59 ± 1.13 in metastatic vs. −0.16 ± 0.67 in nonmetastatic cases; P = 0.001). The measured area under the curve for the value of miRNA-10b was 0.923 (P < 0.001; 95% confidence interval: 0.811–1) with sensitivity and specificity of 100% and 94.4%. Conclusion: Based on this study, metastatic melanoma was associated with elevated levels of miRNA-10b. This marker had the sensitivity and specificity of 100% and 94.4% for the discrimination of metastatic melanoma from nonmetastatic ones.

Bu çalışma, 18-21 Ekim 2018 tarihleri arasında Trabzon[Türkiye]’da düzenlenen 12. Congress of the Turkish-Transplantation-Centers-Coordination-Association (TTCCA)’da bildiri olarak sunulmuştur. Liver transplantation (LT) is the best treatment option for hepatitis B virus (HBV)e mediated hepatocellular carcinoma (HCC). Nevertheless, recurrence is the most important issue after LT. The aims of the present study were to evaluate the relation of dysregulated expression of microRNAs (miRNAs) in recurrence formation in HBV-mediated HCC cases. A total of 42 HBV-mediated HCC patients were evaluated in this study. Among 21 miRNAs, the expression level of miR-106a and miR-21 were higher and miR-143 and miR145 were lower in patients with HCC compared with noncancerous liver tissues (P = .0388, P = .0214, P = .0321, and P = .002, respectively). Compared with nonrecurrent patients, the expression level of miR-21 was 3.54-fold higher and miR-145 was 2.42-fold lower in patients with recurrence during the 5-year follow-up (P = .004 and P = .032; respectively). In addition, according to multivariate Cox regression analysis, the overexpression of miR-21 was found to be a prognostic indicator in HBV-mediated HCC patients (P = .002). In conclusion, we show a significant association between high expression of miR-21 and recurrence in HBV-mediated HCC. Therefore, up-regulation of miR-21 could serve as a promising prognostic marker for HCC. Turkish Transplantat Ctr Coordinat Assoc

Although long noncoding RNA TUC338 has been characterized as an oncogene, its role in bladder cancer is unknown. The purpose of the present study is to investigate the function of TUC338 in bladder cancer. We found that TUC338 was upregulated in early-stage bladder cancer patients and showed early diagnostic values. After surgical resection, plasma levels of TUC338 were significantly downregulated. Moreover, microRNA 10b (miR-10b) was also upregulated in bladder cancer patients. TUC338 and miR-10b were positive and significantly correlated in bladder cancer patients, but not in healthy controls. Bladder cancer cells with TUC338 overexpression showed upregulated miR-10b, while miR-10b overexpression failed to significantly affect TUC338. TUC338 and miR-10b overexpression significantly promoted bladder cancer cell invasion and migration. Therefore, TUC338 may promote bladder cancer at least partially by upregulating miR-10b.

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.

Review on MIR10B (microRNA 10b), with data on DNA, on the protein encoded, and where the gene is implicated.

Several prognostic factors are currently used to stratify breast cancer patients based on the risk of disease progression. However, even patients classified as at low risk can progress and die for the disease. MicroRNA-10b (miR-10b) has a prominent role in regulating tumor invasion and metastasis by targeting the HOXD10 transcriptional repressor and has been found up-regulated in several tumor types including breast cancer. We evaluated the expression of miR-10b in paired tumor and normal specimens obtained from a prospective cohort of breast cancer patients with at least 36 months follow-up enrolled according to the REMARK guidelines (n=150). RNA quality was measured and only samples with RNA Integrity Number (RIN) ≥7.0 were analyzed. The relative expression of miR-10b in tumor as compared to its normal counterpart (RER) was determined by RT-qPCR. miR-10b RERs were higher in the subgroup of patients with synchronous metastases (n=11, Median 0.25; IQR 0.11-1.02) as compared with patients without metastases (n=90, Median 0.09; IQR 0.04-0.29) (p=0.028). In the subgroup of patients without synchronous metastases (n=90), higher miR-10b RERs were associated with increased risk of disease progression and death in both univariable (HR 4.35, p=0.021 and HR 6.02, p=0.015 respectively) and multivariable (HR 13.37, p Our results provide evidences that the addition of miR-10b RERs to the prognostic factors used in clinical routine could improve the prediction abilities for both overall mortality and disease progression in breast cancer patients. Citation Format: Paola Parrella, Raffaela Barbano, Barbara Pasculli, Andrea Fontana, Massimiliano Copetti, Vanna Maria Valori, Maria Luana Poeta, Giuseppe Perrone, Michelina Coco, Teresa Balsamo, Fabio Pellegrini, Andrea Onetti Muda, Evaristo Maiello, Roberto Murgo, Vito Michele Fazio. Evaluation of microRNA-10b prognostic significance in a prospective cohort of breast cancer patients. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1477. doi:10.1158/1538-7445.AM2014-1477

The RNA motifs that bind guanidinylated kanamycin A (G Kan A) and guanidinylated neomycin B (G Neo B) were identified via two-dimensional combinatorial screening (2DCS). The results of these studies enabled the “bottom-up” design of a small molecule inhibitor of oncogenic microRNA-10b.

576 Background: MicroRNA-10b was found highly expressed in metastatic breast cancer cell lines and able to generate metastases in mice models. The aim of this study is to evaluate the putative association between miR10b expression and disease progression. Methods: We selectedfrom our tumor bank 150 consecutive breast cancers with at least three years follow up. For each case frozen paired tumor and normal tissue and complete clinical data were available. Pathological examination was performed to ensure that each tumour sample contained more than 70% of cancer cells resulting in 114 samples suitable for RNA extraction. RNA quality was measured and only samples with RIN≥7.0 were analyzed (n=101) by a relative quantification method. Results: miR10b relative expression in tumor to normal samples (RERs) was significantly higher in the subgroup of patients with metastases (median 0.25 IQR 0.11-1.02) as compared with patients without metastases (median 0.09 IQR 0.04-0.29) (P=0.023 Mann Whitney Test). The association between miR-10b RERs and survival was evaluated in the group of patients without metastases at diagnosis (n=90). In univariate Cox regression model, patients with high miR-10b RERs had a higher risk of distant metastases development (HR 4.91, P=0.02) and disease related death (HR 6.02; P=0.01). In a multivariate Cox regression model adjusted for tumor size, lymph node metastases, grade, ER, PgR status, and Ki67 labeling index (n=79), higher miR-10b RERs were still associated with increased risk of distant metastases development (HR18.84; P

We sought to elucidate the role of a potentially oncogenic microRNA, microRNA-10b (mir-10b), in mediating the pathology of glioblastoma multiforme (GBM). MicroRNAs are small noncoding RNAs that play a critical role in developmental and physiological processes and are implicated in the pathogenesis of several human diseases including cancer. MicroRNAs function by regulating target gene expression post-transcriptionally. We have previously assessed the expression pattern of 241 mature human microRNAs in the NCI60 panel of cell lines and in a set of corresponding normal tissues (Gaur et al., 2007, Cancer Research. 67(6):2456-68). We found that microRNA expression patterns mark specific biological characteristics of tumors and/or mediate biological activities important for their pathobiology. In CNS tumor-derived cell lines, we identified mir-10b as a candidate oncogene, as it is expressed at higher levels in human GBM lines an primary GBM tissue than it is in normal brain tissue. Using several target prediction algorithms we identified a member of the homeobox family, Homeobox D10 (HOXD10), as a potential target of mir-10b. Our in vitro studies demonstrate that down regulation of mir-10b in GBM-derived cell lines results in increased expression levels of HOXD10. Additionally, our data indicate that down-regulation of mir-10b in human GBM lines leads to decreased proliferation and decreased anchorage independent colony formation in soft agar. Importantly, using a xenograft model in immune-deficient nude mice, we have observed human that GBM lines in which mir-10b expression is inhibited exhibit decreased tumor formation and growth in vivo. Furthermore, the decreased colony formation in soft agar observed as a result of mir-10b inhibition in GBM-derived cell lines is significantly antagonized by expression of siRNAs complementary to HOXD10 mRNA. Also, over expression of HOXD10 in GBM cell lines results in differentiation and decreased proliferation. Further experiments are ongoing to identify the specific role of HOXD10 in mediating the pathologic characteristics of GBM. An understanding of the pathways mediated by HOXD10 signaling may provide novel opportunities for therapeutic intervention. The National Brain Tumor Society (ABG) and the Theodora B. Betz Foundation (MAI) supported this work. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2100.

Arising from: L. Ma, J. Teruya-Feldstein & R. A. Weinberg , 682–688 (2007)10.1038/nature06174 ; Ma et al. reply MicroRNAs regulate messenger RNA expression but are frequently dysregulated in tumours. Ma et al.1 report that overexpression of microRNA-10b (miR-10b) initiates invasion and metastasis in models of breast cancer and that its expression in primary breast carcinomas correlates with clinical progression. We tested this in patients with primary breast cancer, of whom 92 had nodal metastases at diagnosis and 127 were node-negative. We found no significant association between miR-10b levels and metastasis or prognosis. Although we concede that miR-10b may have a biological effect in a few cells at the growing edge of a tumour, we believe that it is unlikely to correlate in whole tumour samples with clinical progression.