DNA Methylation and Chromatin Accessibility Impact Subgenome Expression Dominance in the Common Carp (Cyprinus carpio).

DNA methylation and chromatin accessibility play important roles in gene expression, but their function in subgenome expression dominance remains largely unknown. We conducted comprehensive analyses of the transcriptome, DNA methylation, and chromatin accessibility in liver and muscle tissues of allotetraploid common carp, aiming to reveal the function of epigenetic modifications in subgenome expression dominance. A noteworthy overlap in differential expressed genes (DEGs) as well as their functions was observed across the two subgenomes. In the promoter and gene body, the DNA methylation level of the B subgenome was significantly different than that of the A subgenome. Nevertheless, differences in DNA methylation did not align with changes in homoeologous biased expression across liver and muscle tissues. Moreover, the B subgenome exhibited a higher prevalence of open chromatin regions and greater chromatin accessibility, in comparison to the A subgenome. The expression levels of genes located proximally to open chromatin regions were significantly higher than others. Genes with higher chromatin accessibility in the B subgenome exhibited significantly elevated expression levels compared to the A subgenome. Contrastingly, genes without accessibility exhibited similar expression levels in both subgenomes. This study contributes to understanding the regulation of subgenome expression dominance in allotetraploid common carp.

Rapid and Non-Invasive Assessment of Texture Profile Analysis of Common Carp (Cyprinus carpio L.) Using Hyperspectral Imaging and Machine Learning.

Hyperspectral imaging (HSI) has been applied to assess the texture profile analysis (TPA) of processed meat. However, whether the texture profiles of live fish muscle could be assessed using HSI has not been determined. In this study, we evaluated the texture profile of four muscle regions of live common carp by scanning the corresponding skin regions using HSI. We collected skin hyperspectral information from four regions of 387 scaled and live common carp. Eight texture indicators of the muscle corresponding to each skin region were measured. With the skin HSI of live common carp, six machine learning (ML) models were used to predict the muscle texture indicators. Backpropagation artificial neural network (BP-ANN), partial least-square regression (PLSR), and least-square support vector machine (LS-SVM) were identified as the optimal models for predicting the texture parameters of the dorsal (coefficients of determination for prediction (rp) ranged from 0.9191 to 0.9847, and the root-mean-square error for prediction ranged from 0.1070 to 0.3165), pectoral (rp ranged from 0.9033 to 0.9574, and RMSEP ranged from 0.2285 to 0.3930), abdominal (rp ranged from 0.9070 to 0.9776, and RMSEP ranged from 0.1649 to 0.3601), and gluteal (rp ranged from 0.8726 to 0.9768, and RMSEP ranged from 0.1804 to 0.3938) regions. The optimal ML models and skin HSI data were employed to generate visual prediction maps of TPA values in common carp muscles. These results demonstrated that skin HSI and the optimal models can be used to rapidly and accurately determine the texture qualities of different muscle regions in common carp.

Extremely high serum CA19-9 level along with elevated D-dimer in assisting detection of ruptured ovarian endometriosis.

BACKGROUND: To clarify clinical importance of serum CA19-9, CA-125, and plasma D-dimer (D-D) levels in detecting spontaneously ruptured ovarian endometriosis (OE). MATERIALS AND METHODS: We retrospectively examined 173 patients with endometriosis out of 735 cases of OE between 2013 and 2019. Among these, 21 cases were diagnosed as "spontaneously ruptured" after surgery, while the remaining cases were unruptured. Venous blood was collected pre-operatively to detect CA19-9, CA-125, and D-D levels. A receiver operating characteristic curve analysis was applied to test clinical value of each marker. RESULTS: Among the 21 patients with ruptured OE, 16 had a history of pelvic cysts, 19 claimed sudden onsets of lower abdominal pain, and fluid accumulation were detected in cul-de-sac in only six participants by ultrasound. For serological investigation, both CA19-9 and D-D were significantly elevated in the ruptured OE group (343.09 ± 367.67 U/ml vs. 36.84 ± 40.01 U/ml, 3.39 ± 4.90 mg/L vs. 0.43 ± 0.29 mg/L, both p < .0001). The area under curve (AUC) value for the combination of CA19-9 and D-D was 0.975 (95% CI, 0.939 - 0.993), with specificity of 96.69%, and sensitivity of 85.71%. The combination of CA-125, CA19-9 and D-D showed the highest AUC value that up to 0.976 (95% CI, 0.940-0.993), with sensitivity of 95.24%, and specificity of 87.50%. CONCLUSION: The combination of CA19-9 and D-D can be chosen as an effective and economical indicators to identify patients with spontaneously ruptured OE in pre-operation assessment. However, from the perspective of differential diagnosis, the combination of CA-125, CA19-9 and D-D is the best choice. Key messagesTaking into account the economic effect, the combination of CA19-9 and D-D can be chosen as an effective indicators to identify patients with spontaneously ruptured OE in pre-operation assessment.From the perspective of differential diagnosis, the combination of CA-125, CA19-9 and D-D is the best choice to identify patients with spontaneously ruptured OE.

Targeted delivery of exosomal miR-484 reprograms tumor vasculature for chemotherapy sensitization.

The vascular dysfunction of ovarian cancer (OC) contributes to the chemotherapeutic resistance. In this study, we aimed to explore whether exosome-mediated angiogenesis blocking could improve the chemotherapy sensitivity via vascular normalization. Exosomes were armed with RGD on the surface by fusing Lamp2b. Candidate miRNAs related to tumor angiogenesis was detected by qRT-PCR. RGD-modified exosomes were loaded with miRNAs via electroporation. The therapeutic effects of the exosomes on angiogenesis, vascular normalization, and chemotherapy sensitivity were systemically analyzed in the xenograft model. RGD-modified exosomes were relatively enriched in the tumor mass, both the tumor cell and the endothelial cells. Among the miRNA candidates, miR-484 was found down-regulated in both the cancer cells and the angiogenic endothelial cells. In vivo xenograft model experiment revealed that injection of RGD-modified exosomes loaded with miR-484 induced vessel normalization and in turn sensitized the cancer cells to chemotherapy induced apoptosis. Mechanistically, miR-484 simultaneously inhibited the expression of VEGF-A from the cancer cells and the corresponding receptors in the endothelial cells. Targeted delivery of miR-484 via RGD-modified exosomes improves the vascular normalization, sensitizes the cancer to chemotherapy, and prolongs the survival time of tumor-bearing mice after chemotherapy, opening an avenue for the clinical management of chemotherapy resistance.

Dysregulation of lnc-SNHG1 and miR-216b-5p correlate with chemoresistance and indicate poor prognosis of serous epithelial ovarian cancer.

AIM: This study aimed to explore whether the dysregulation of lnc-small nucleolar RNA host gene 1 (SNHG1) and miR-216b-5p correlated with chemoresistance and indicated poor prognosis of serous epithelial ovarian cancer (EOC). METHODS AND RESULTS: The expression of lnc-SNHG1 was upregulated, while miR-216b-5p showed low expression in patients with chemoresistant EOC compared with patients with chemosensitive EOC. The multivariate Cox regression analysis showed that the expression of miR-216b-5p and FIGO stage were independent prognostic factors for the overall survival (OS) of patients with serous EOC. Kaplan-Meier curves revealed a significant association of the increased expression level of lnc-SNHG1 with shorter OS and disease-free survival (DFS). Patients with a low expression level of miR-216b-5p also had shorter OS and DFS. The biological functions were tested using CCK-8 assay, colony formation assay, wound healing assay, and cell apoptosis. The knockdown of SNHG1 and the overexpression of miR-216b-5p stimulated paclitaxel sensitivity in A2780/Taxol cells through inhibiting cell growth and migration and promoting apoptosis. The inhibition of miR-216b-5p could rescue the effect of lnc-SNHG1 inhibition on the sensitivity of A2780/Taxol cells to paclitaxel. Luciferase reporter assay, RNA Binding Protein Immunoprecipitation Assay (RIP), and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) indicated that lnc-SNHG1 acted as a sponge of miR-216b-5p in A2780/Taxol cells. CONCLUSIONS: This study showed that the overexpression of lnc-SNHG1 and decreased expression level of miR-216b-5p correlated with the chemoresistance of patients with serous EOC and indicated shorter OS and DFS. Lnc-SNHG1 functioned as a ceRNA with miR-216b-5p, which was critical in modulating the paclitaxel sensitivity of ovarian cancer cells.

MiR-1307 influences the chemotherapeutic sensitivity in ovarian cancer cells through the regulation of the CIC transcriptional repressor.

BACKGROUND: Extended from our previously observation that expression of miR-1307 in chemoresistant primary ovarian cancer tissues is elevated, here we are aiming to dissect the function of miR-1307 and its predicted target gene, CIC (capicua transcriptional repressor), in ovarian cancer chemotherapy. METHODS: We evaluated the expression of miR-1307 and CIC in chemoresistant and chemosensitive ovarian cancer tissues and cells by real time-PCR and western blot. We used chemoresistant/chemosensitive cells with miR-1307 suppression/overexpression to study the biological effects of miR-1307 by MTT and flow cytometer. Dual luciferase reporter gene assay was used to validate direct binding between miR-1307 and the 3'-UTR of CIC. Real-time PCR and western blot analyses, MTT and flow cytometry were used to reveal the biological effects of miR-1307 and CIC, as well as their regulation. RESULTS: We found that miR-1307 affects cell cycle dynamics, cell viability in ovarian cancer cells. In addition, its expression level can influence chemosensitivity to paclitaxel in ovarian cancer cells. We also validate that CIC is a downstream target of miR-1307 via its regulation on 3'-UTR of CIC gene and ETV4 and ETV5 are also regulated by miR-1307/CIC axis. CONCLUSIONS: Our data suggested that miR-1307 may be involved in the resistance of ovarian cancer to chemotherapy drugs via regulation of CIC, and should be further explored as a potential therapeutic target.

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Nitrogen balance index (NBI) is one of the important indicators for crop growth. The high and low status of nitrogen can be quickly monitored by measuring NBI, which can provide accurate information of agricultural production and management. The relationship between NBI and original spectrum and derivative spectrum of infrared and near infrared wavelength from flowering to maturity stage was analyzed based on high definition digital image and hyperspectral data on unmanned aerial vehicles. Then, the sensitive bands were selected and the vegetation indexes were calculated. The inversion models of NBI were constructed by empirical model method. The optimal inversion model was obtained by analysing the determination coefficient (R2) and the root mean square error (RMSE) of validating model. The results showed that the correlation between NBI and derivative spectral reflectance was more stronger than that between it and original spectral reflectance. All the 14 vegetation indices selected in this study, except the derivative spectral photochemical reflectance index, had significant correlation with NBI. The NBI inversion models were constructed based on those 13 vegetation indices and the accuracy was analyzed. The inversion model constructed by derivative spectral difference vegetation index had the highest accuracy, with the R2 and RMSE being 0.771 and 3.077 respectively. The soybean NBI distribution maps of the whole growing stages generated by this model could reflect the soybean growth state. Estimation of NBI using the high definition digital image and hyperspectral data obtained by unmanned aerial vehicle, as shown by our results, could be a real-time, dynamic, non-destructive and effective way to monitor the nitrogen status of soybean. It's a simple and practical method for precise management of nitrogen in soybean.

Up-Regulation of Long Noncoding RNA SRA Promotes Cell Growth, Inhibits Cell Apoptosis, and Induces Secretion of Estradiol and Progesterone in Ovarian Granular Cells of Mice.

BACKGROUND Increasing evidence indicates that long noncoding RNAs (LncRNAs) play a key role in multiple pathological processes. It has been shown that LncRNA steroid receptor RNA activator (SRA) is elevated in peripheral blood of patients with polycystic ovary syndrome (PCOS). The aim of this study was to assess the effect of elevated LncRNA SRA on ovarian granular cells of mice in vitro. MATERIAL AND METHODS We firstly isolated granular cells from mouse ovaries and over-expressed the LncRNA SRA by means of lentiviral transfection in this cell line. Then, we assessed the effects of LncRNA SRA on granular cells through real-time PCR, CCK-8 assay, flow cytometry, Hoechst staining, and Western blot assay. RESULTS We demonstrated that elevated LncRNA SRA stimulated cell growth, changed distribution of cell cycle phases with increase of Cyclin B, Cyclin E, and Cyclin D1, and inhibited cell apoptosis with up-regulation of bcl2 and down-regulation of bax, cleaved-caspase 3, and cleaved-PARP. Moreover, the contents of estradiol (E2) and progesterone (PG) and expressions of their key enzymes (CYP19A1 and CYP11A1) were up-regulated following over-expression of LncRNA SRA. CONCLUSIONS Taken together, our results indicate that abnormal LncRNA SRA may be a risk factor for evoking PCOS.

NF-κB1, c-Rel, and ELK1 inhibit miR-134 expression leading to TAB1 upregulation in paclitaxel-resistant human ovarian cancer.

The mechanism by which the transcription factors inhibit the miRNA expression in ovarian cancer chemoresistance is unclear. The present study investigated the mechanism underlying the transcriptional repression of miR-134 in chemoresistant serous epithelial ovarian cancer. The results demonstrate that NF-κB1, c-Rel, and ELK1 are involved as transcription factors in repressing miR-134 expression in paclitaxel-resistant ovarian cancer cells. Knockdown of these transcription factors led to increased miR-134 expression, resulting in increased apoptosis and inhibition of proliferation in SKOV3-TR30 cells. NF-κB1, c-Rel, and ELK1 mRNA expression was upregulated in chemoresistant specimens and negatively correlated with miR-134 expression. Kaplan-Meier analysis revealed that high nuclear expressions of NF-κB1, c-Rel, ELK1 were significantly associated with short survival in serous epithelial ovarian cancer patients. Finally, TAB1 was identified as a functional target of miR-134, and the expression of TAB1 was increased by the transcription factors of NF-κB1, c-Rel, and ELK1 via miR-134. Taken together, these results provide an insight into the mechanism of repressed miR-134 expression in chemoresistance of serous epithelial ovarian cancer.

Over-expression of nuclear NF-κB1 and c-Rel correlates with chemoresistance and prognosis of serous epithelial ovarian cancer.

OBJECTIVE: This study aims to measure the expression and subcellular location of NF-κB1 and c-Rel protein in serous epithelial ovarian cancer (EOC), and to test the correlation between NF-κB1 and c-Rel expression and clinicopathological parameters, chemoresistance, and prognosis of serous EOC. METHODS: A total of 63 specimens of serous EOC patients meeting the inclusion criteria with complete follow-up data were enrolled in our study. The specimens were divided into chemo-resistant group and sensitive group. The expression and subcellular location of NF-κB1 and c-Rel were assessed in paraffin sections using immunohistochemistry. The relationship between NF-κB1 and c-Rel protein expression and pathological characteristics of serous EOC, chemoresistance, prognosis and survival time was analyzed. RESULTS: The positive nuclear staining of NF-κB1 and c-Rel were significantly higher in the chemo-resistant serous EOC specimens than that in chemo-sensitive group. Lymph node metastasis and the nuclear expression of NF-κB1 and c-Rel were independent risk factors associated with chemotherapy resistance of serous EOC. Nucleus NF-κB1 and c-Rel expression along with FIGO stage were independent risk factors that strongly correlated with prognosis of serous EOC. Western blot result showed the protein level of NF-κB1 and c-Rel was significantly higher in chemoresistant group compared with in sensitive group. CONCLUSIONS: Over-expression of nuclear NF-κB1 and c-Rel are strong risk factors associated with chemoresistance and the prognosis of serous epithelial ovarian cancer.

Over-expression of Sirt1 contributes to chemoresistance and indicates poor prognosis in serous epithelial ovarian cancer (EOC).

Ovarian cancer is the most lethal malignancy in female patients, and chemoresistance is the major contribution to low over survival rate. We aim to investigate the correction between Sirt1 expression and chemoresistance in serous epithelial ovarian cancer (EOC) and prognosis significance of Sirt1. Immunochemistry was used to determine the location pattern and expression of Sirt1 in a total of 63 serous EOC patients (28 cases of chemoresistance patients and 35 chemosensitive).The relationship between Sirt1 expression and clinicopathological features of serous EOC was analyzed. Univariate analysis and multifactor logistic regression analysis were applied to investigate risk factor for chemoresistance. Cox proportional hazards regression model and Kaplan-Meier survival analysis were applied to determine the prognosis factor and survival time. Immunohistochemistry proved that over-expression of nuclear Sirt1 was related to chemoresistance (P = 0.039). Multivariate logistic regression analysis proved that the nuclear expression of Sirt1 (P = 0.018) and the lymph node metastasis (P = 0.037) was independent risk factors for chemoresistance in serous epithelial ovarian cancer. Multivariate Cox regression result indicated that expression of Sirt1 (P = 0.026, RR 2.434, 95 % CI 1.109-5.339) and stage (P = 0.005, RR 2.366, 95 % CI 1.288-4.345) was independent prognostic factors. Kaplan-Meier analysis showed that the survival rate is significantly decreased in the Sirt1 highly expressed group. Western blot result showed that the protein level of Sirt1 was significantly higher in chemoresistant group compared with in sensitive group. In conclusion, our results proved that over-expression of Sirt1 could play an important role in chemoresistance of serous EOC and could be a prognosis indicator for the patient's survival outcome.

Down-regulated expression of miR-134 contributes to paclitaxel resistance in human ovarian cancer cells.

MiR-134 has been reported to have a role in the development and progression of various cancers. In this study, we found that miR-134 expression was significantly decreased in chemo-resistant serous epithelial ovarian cancer (EOC) patients. Over-expression of miR-134 enhanced the sensitivity of SKOV3-TR30 cells to paclitaxel, and increased paclitaxel-induced apoptosis. Further, Pak2 was identified as a direct target of miR-134, and Pak2-specific siRNA increased cell inhibition rate and promoted paclitaxal-induced apoptosis. By regulating Pak2 expression, miR-134 could mediate Bad phosphorylation at Ser112 and Ser136, which affected cell survival and apoptosis. In conclusion, our findings indicate that repression of miR-134 and consequent up-regulation of Pak2 might contribute to paclitaxel resistance.

Hybrid-polymerase chain reaction to identify novel target genes of miR-134 in paclitaxel resistant human ovarian carcinoma cells.

Increasing evidence has shown that miR-134 is involved in the promotion of tumorigenesis and chemoresistance. However, whether miR-134 participates in ovarian cancer chemoresistance and its functional targets still remains unclear. The objective of this study was to apply hybrid-polymerase chain reaction (PCR) to screen target genes of miR-134 in ovarian carcinoma paclitaxel resistant SKOV3-TR30 cells, and to provide a number of novel targets of miR-134 for further study of ovarian cancer paclitaxel resistance. The current study found that miR-134 was decreased in SKOV3-TR30 cells compared with the parental SKOV3 cell line. By applying hybrid-PCR, 8 putative target genes of miR-134 in SKOV3-TR30 cells were identified, including C16orf72, PNAS-105, SRM, VIM, F-box protein 2, GAPDH, PRPF6 and RPL41. Notably, the target sites of VIM and PRPF6 were not located in 3'untranslated region, but rather in the coding sequence region. By conducting a luciferase reporter assay, miR-134 was demonstrated to recognize the putative binding sites of these target genes including VIM and PRPF6. Transfecting SKOV3-TR30 cells with miR-134 mimic and performing reverse transcription-PCR in addition to western blot analysis confirmed that miR-134 regulates vimentin expression at a post transcriptional level. This finding provides a novel perspective for studying the mechanism of miR-134/mRNA interaction. In conclusion, this study was the first to apply an effective method of hybrid-PCR to screen putative target mRNAs of miR-134 in paclitaxel resistant SKOV3-TR30 cells and indicate that miR-134 may contribute to the induction of SKOV3-TR30 paclitaxel resistance by targeting these genes.

The clinicopathological significance of miR-1307 in chemotherapy resistant epithelial ovarian cancer.

BACKGROUND: We aimed to examine the expression of miR-1307 in chemosensitive and chemoresistant epithelial ovarian cancer tissues and cell lines and to analyze the clinicopathological significance of miR-1307 in ovarian cancer. METHODS: MicroRNA microarray was used to screen differentially expressed microRNAs between the chemosensitive and chemoresistant epithelial ovarian cancer tissues. RT-PCR was used to validate the candidate microRNA. The potential target genes and their enriched biological pathways of microRNA were also analyzed. Dual Luciferase Reporter Gene Assay was conducted to validate the regulation of miRNA-1307 on the 3'-UTR of DAPK3. RESULTS: miRNA-1307 was up-regulated in the chemoresistant epithelial ovarian cancer tissues compared to the chemosensitive counterparts. The up-regulation of miRNA-1307 was not associated with menopause, tumor differentiation state, clinical stage, and lymph node metastasis of ovarian cancer. Gene ontology analysis of miR-1307 candidate target genes indicated that miR-1307 candidate target genes were enriched in the processes of cell proliferation and differentiation, nucleotide synthesis and metabolism, and lymphocytes activation. CONCLUSION: Our results suggest that miRNA-1307 may play a role in the development of chemoresistance in ovarian cancer.

Myricetin suppresses differentiation of 3 T3-L1 preadipocytes and enhances lipolysis in adipocytes.

Myricetin (MyR), a naturally occurring flavonol widely distributed in fruits, vegetables, and medicinal plants, has anticancer, anti-inflammatory, antihyperlipidaemic, and antiobesity activities. In the present study, we hypothesized that the antiobesity property of MyR is mediated via suppression of differentiation of preadipocytes into adipocytes and promotion of lipolysis of mature adipocytes, which effectively decrease the intracellular triglyceride concentration of adipocytes. Accordingly, the aim of this work was to investigate the effects of MyR on adipocyte differentiation and lipolysis in differentiated 3 T3-L1 adipocytes. Our results showed that MyR inhibited differentiation of 3 T3-L1 preadipocytes in a concentration-dependent manner. Myricetin downregulated the mRNA and protein levels of CCAAT/enhancer-binding protein α and peroxisome proliferator-activated receptor γ, both of which are major adipogenic transcription factors. Furthermore, the mRNA levels of other adipogenesis-related transcription factors, namely, CCAAT/enhancer-binding protein ß, sterin regulatory element binding protein 1-c, peroxisome proliferator-activated receptor γ coactivator-1, adipocyte protein 2, lipoprotein lipase and glucose transporter 4, were also reduced by MyR treatment. Moreover, MyR significantly inhibited the phosphorylation of extracellular signal-regulated kinase, Jun N-terminal kinase, and p38 during the differentiation process. On the other hand, MyR induced a dose-dependent increase in glycerol release in fully differentiated adipocytes, indicating its stimulatory effect on adipocyte lipolysis. Furthermore, MyR downregulated mRNA level of perilipin A and enhanced the phosphorylation level of extracellular signal-regulated kinase, Jun N-terminal kinase, and p38 during lipolysis. Taken together, these findings indicate that MyR exerts antiobesity activity in adipocytes.

Expression of the ELAV-like protein HuR in the cytoplasm is associated with endometrial carcinoma progression.

Human antigen R (HuR) is an mRNA-binding factor that belongs to the embryonic lethal abnormal vision/Hu protein family which may function as a tumor maintenance gene in a variety of carcinomas. However, there is no study to analyze HuR expression in endometrial carcinoma. Here, we investigated the expression of HuR in endometrial carcinoma carcinogenesis and subsequent progression. The expression of HuR and estrogen receptor alpha (ER-α) protein was examined by immunohistochemistry on paraffin embedding specimens containing endometrial carcinoma and adjacent non-cancerous tissues. Short hairpin RNA against HuR was transfected to investigate the role of HuR in regulating the expression of ER-α and progression in endometrial carcinoma. Cell viability and cycle were measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry, respectively. Apoptosis was examined by annexin V apoptosis assay. Our study result show that cytoplasmic HuR expression is more frequent in poorly differentiated carcinomas (p = 0.005), advanced stage (p = 0.020), and positive ER-α expression (p = 0.026). Three HuR short hairpin RNAs (shRNAs) were transfected into Ishikawa cells, and we selected the most effective shRNA for the following experiments. After the transfection, the ER-α protein level was decreased. Further, decreased expression of HuR resulted in the inhibition of proliferation and induced apoptosis in Ishikawa cells. Our results showed that HuR could be a causal factor of ER-α regulation in Ishikawa cells and thus may induce the hormone-dependent endometrial carcinoma.

Downregulation of miR-17~92 Expression Increase Paclitaxel Sensitivity in Human Ovarian Carcinoma SKOV3-TR30 Cells via BIM Instead of PTEN.

To better understand the molecular mechanisms of paclitaxel resistance in ovarian carcinoma, we evaluated the expression of miRNAs using miRNA microarray between human ovarian carcinoma SKOV3 cells and paclitaxel resistant SKOV3-TR30 cells. Results showed that 69 miRNAs were upregulated while 102 miRNAs were downregulated in SKOV3-TR30 cells. Using real-time PCR, we further clarified that miR-17~92 was overexpressed in SKOV3-TR30 cells compared with that in SKOV3 cells. We then established stable virally transduced SKOV3-TR30-m-PTIP-Sponge all SKOV3-TR30 cells and its vector-only control SKOV3-TR30-m-PTIP-GFP cells. Real time-PCR revealed that SKOV3-TR30-m-PTIP-Sponge all cells expressed approximately 6.18-fold lower levels of miR-17~92 compared with the control group. Decreased expression of miR-17~92 resulted in cell cycle arrest in the G2/M phase and growth inhibition. After the transduction, the BIM protein level was increased in SKOV3-TR30 cells and luciferase reporter assays revealed that miR-17~92 binds directly to the 3'-UTR of BIM. Results of luciferase reporter assays accompanied with Western Blot showed that although miR-17~92 binds directly to the 3'-UTR of PTEN, the PTEN protein expression level was upregulated slightly while the result is of no statistical significance. Our results showed that miR-17~92 could be a causal factor of the downregulation of BIM in SKOV3-TR30 cells and thus induce the paclitaxel resistance in SKOV3-TR30 cells.