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Currently, circular RNAs (circRNAs) have been demonstrated to play vital roles in malignant tumors, including glioma. Nevertheless, the functions of circTTBK2 in glioma are largely unclear.

Quantitative real-time polymerase chain reaction (qRT-PCR) was applied for the expression levels of circTTBK2, TTBK2 mRNA, miR-145-5p and cytoplasmic polyadenylation element binding protein 4 (CPEB4) mRNA. Actinomycin D and RNase R digestion assays were utilized for the characteristics of circTTBK2. 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay, flow cytometry analysis and transwell assay were conducted for cell proliferation, apoptosis and metastasis, respectively. The glycolysis level was estimated with specific kits. Western blot assay was adopted for the protein levels of hexokinase2 (HK2) and CPEB4. The targeting relationship between miR-145-5p and circTTBK2 or CPEB4 was verified by Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Murine xenograft assay was used for the role of circTTBK2 in tumorigenesis in vivo.

CircTTBK2 was upregulated in glioma tissues and cells, and its level was associated with poor survival of glioma patients. CircTTBK2 knockdown suppressed glioma cell proliferation, migration, invasion and glycolysis and accelerated apoptosis in vitro and hampered tumor growth in vivo. CircTTBK2 functioned as a sponge of miR-145-5p, and miR-145-5p inhibition restored the effects of circTTBK2 knockdown on the malignant behaviors of glioma cells. Moreover, CPEB4 was the direct target gene of miR-145-5p, and miR-145-5p inhibition facilitated glioma cell progression by targeting CPEB4.

CircTTBK2 functioned as a tumor promoter in glioma by modulating miR-145-5p/CPEB4 axis, which might offer a new sight for glioma therapy.

CircTTBK2 functioned as a tumor promoter in glioma by modulating miR-145-5p/CPEB4 axis, which might offer a new sight for glioma therapy.

The predictive value of anti-Müllerian hormone (AMH) for ovarian dysfunction postchemotherapy is controversial. This study aimed to evaluate the value of serum AMH levels clinically and theoretically.

We detected the serum estradiol, follicular stimulating hormone (FSH), luteinizing hormone (LH), and AMH levels in 144 premenopausal women with breast cancer receiving cyclophosphamide-based chemotherapy. The hormone levels before and postchemotherapy were compared; the correlations among the hormones and amenorrhea and menstrual recovery were analyzed. In addition, the serum AMH levels were detected randomly in 177 normal healthy women and 36 normal female C57BL/6J mice of different ages; meanwhile, the status of ovarian follicles was also examined. Furthermore, 72 Balb/c nude mice with breast cancer were randomly assigned to three groups that received different doses of cyclophosphamide (CTX) (control, 100 mg/kg, and 200 mg/kg), and the alterations in serum AMH levels and ovarian follicles were recorded anr predicting postchemotherapy ovarian function exclusively in premenopausal female patients with breast cancer aged >35 years.

35 years.

This study aimed to evaluate the regulatory role of miR-431-5p on the tumorigenesis of osteosarcoma (OS) and the underlying mechanism involving

(

).

qRT-PCR was applied to measure the expression of miR-431-5p in OS tissues and cells.

and miR-431-5p were overexpressed in U2OS and HOS cells. Fluorofurimazine The cell viability and apoptosis were determined by MTT and FITC/PI double staining assay, respectively. Transwell assay was performed to detect cell migration and invasion. The protein expression of cleave-caspase-3 and MMP-2/-9 was detected by Western blot. The target relationship between miR-431-5p and

was predicated by ENCORI and identified by DLR assay. The anti-tumor effect of miR-431-5p was further analyzed in a xenograft tumor model in mice.

MiR-431-5p expression was down-regulated in OS tissues and negatively correlated with lymph node metastasis and TNM stage. Over-expression of miR-431-5p induced cell apoptosis, inhibited cell proliferation, migration and invasion, up-regulated cleave-caspase-3, and down-regulated MMP-2 and -9 in OS cells. Over-expression of miR-431-5p also inhibited the growth of tumor xenografts in mice. In addition,

was a target of miR-431-5p. Over-expression of

reversed the anti-tumor effect of miR-431-5p mimics on U2OS and HOS cells.

Up-regulation of miR-431-5p suppressed the tumorigenesis of OS via targeting

.

Up-regulation of miR-431-5p suppressed the tumorigenesis of OS via targeting PANX3.

Data about the prognostic value of fibrinogen concentration and absolute lymphocyte count for the prognosis of gastrointestinal stromal tumors (GISTs) were limited. Thus, the aim of the present study was to investigate the predictive value of preoperative fibrinogen concentration and absolute lymphocyte count in GISTs.

From March 2002 to December 2017, 143 intermediate and high risk GIST patients treated with R0 resection were enrolled in the present study. Clinicopathological characteristics were recorded. The optimal cut-off values of patients were calculated by X-tile software. Categorical variables were analyzed using Chi-square test or Fisher's exact test. Disease-free survival was analyzed by the Kaplan-Meier method and compared by a Log rank test.

There were 71 males (49.65%) and 72 females. The median age was 56 years (range 19-86). The optimal cut-off value was 4.5 g/L for fibrinogen concentration (P=0.000) and 1.0×10

/L for lymphocyte count (P=0.002). No significant association was found betwnd high risk GIST patients. The combination of fibrinogen concentration and absolute lymphocyte count could further increase the predictive value for the prognosis of GIST patients.

Increasing evidence suggests that microRNAs (miRNAs) play critical roles in cancer progression. Therefore, investigating the function of miRNAs that are aberrantly expressed in gastric cancer (GC) and characterizing the involved underlying mechanism are essential for the treatment of gastric cancer. MiR-138-5p was found to be down-regulated in multiple cancers, which acted as a tumor suppressor in cancer progression; however, whether and how miR-138-5p regulates the malignant behaviors of GC has not been fully understood.

The level of miR-138-5p in GC tissues and cell lines was detected by RT-qPCR. The effects of miR-138-5p on the growth of GC cells were evaluated by the in vitro Cell Counting Kit-8 (CCK-8) assay, cell apoptosis, cell cycle analysis, wound-healing assay, and in vivo xenograft mice model. The targets of miR-138-5p were predicted using the miRDB online tool, confirmed by luciferase report assay and Western blot.

MiR-138-5p was frequently decreased in GC tissues and cell lines. Decreased expression of miR-138-5p was significantly associated with the lymph node metastasis of GC patients.