Vincentpanduro6657

Introduction Bruton's tyrosine kinase (BTK) inhibitors have long been known in the treatment of B-cell malignancies. Recently, BTK inhibitors have also become promising novel treatment reagents for prostate cancer. The current study was designed to investigate expression of BTK in prostate cancer tissues in comparison with benign hyperplasia and effect of BTK inhibitor on prostate cancer cell proliferation, migration and invasion. Methods BTK expression was assessed by immunohistochemistry; migration and invasion prostate cancer cell lines (DU145 and PC3) were assessed by Transwell migration and wound-healing assay; cancer cell proliferation was assessed using MTT assay kit; expression of matrix metalloproteinases-2 and -9 (MMP-2 and MMP-9) was assessed by immunoblotting. Results Strong expression of BTK was detected in the prostate cancer tissues, especially in the tumors from prostate cancer patients with bone metastasis. BTK inhibitor (Ibrutinib) significantly inhibited cell proliferation, migration and invasion of prostate cancer cells as well as protein synthesis of MMP-2 and MMP-9 by the tumor cells. Overexpressing BTK could partially but significantly block the inhibitory effect of Ibrutinib on cell proliferation, migration and invasion, and protein synthesis of MMP-2 and MMP-9 of the cancer cells. Conclusion These findings suggested that BTK could serve as not only a biomarker but also a therapeutic target for the prostate cancer and that Ibrutinib may be applied as a therapeutic drug for the prostate cancer.Purpose This study aimed to investigate the regulatory role and mechanism of microRNA-766 (miR-766) on cutaneous squamous cell carcinoma (CSCC) cells. Methods The expression of miR-766 and programmed cell death 5 (PDCD5) was detected in CSCC tissues and CSCC cell lines (A431, SCL-1 and DJM-1 cells) by qRT-RCR. The proliferation, colony-forming ability, apoptosis, migration and invasion of A431 and SCL-1 cells was measured by MTT, colony formation, flow cytometry, wound healing and transwell assay, respectively. The interaction between miR-766 and PDCD5 was detected by dual-luciferase reporter gene assay. The expression of matrix metalloproteinase 2 (MMP-2), MMP-9 and PDCD5 was measured by Western blot. In addition, A431 cells were subcutaneously injected into mice, and the tumor volume and weight were measured. Results MiR-766 was upregulated, and PDCD5 was downregulated in CSCC tissues and cells. MiR-766 significantly promoted the proliferation, migration and invasion, and inhibited the apoptosis of A431 and SCL-1 cells. MiR-766 also significantly increased the expression of MMP-2 and MMP-9 in A431 and SCL-1 cells. PDCD5 was a target gene of miR-766. PDCD5 significantly reversed the tumor-promoting effect of miR-766 on A431 and SCL-1 cells. In addition, miR-766 inhibitor inhibited the tumor growth in mice. Conclusion MiR-766 inhibitor inhibited the proliferation, migration and invasion, and promoted the apoptosis of CSCC cells via downregulating PDCD5.Background Paclitaxel (PTX) resistance is a main obstacle for the treatment of triple-negative breast cancers (TNBC). Evidences have shown that miR-153-5p could induce the apoptosis of breast cancer cells. Thus, this study aimed to investigate the effect of miR-153-5p on PTX-resistance TNBC cells. Methods Cell Counting Kit-8, flow cytometry and wound healing assays were used to detect the viability, apoptosis and migration of MDA-MB-231/PTX cells, respectively. The luciferase reporter assay was used to explore the potential binding targets of miR-153-5p. The expressions of CDK1, cyclin B1 and p-Akt in MDA-MB-231/PTX cells were detected with Western blot. In vivo animal study was performed finally. Results In this study, the inhibitory effects of PTX on the proliferation and migration of MDA-MB-231/PTX cells were significantly enhanced following transfection with miR-153-5p. In addition, overexpression of miR-153-5p markedly enhanced the pro-apoptotic effect of PTX on MDA-MB-231/PTX cells. Luciferase reporter assay validated that cyclin-dependent kinase 1 (CDK1) was a potential binding target of miR-153-5p. Moreover, overexpression of miR-153-5p prominently increased PTX-induced cell cycle arrest at G2/M phase in MDA-MB-231/PTX cells via downregulation of CDK1, cyclin B1 and p-Akt. In vivo experiments confirmed that overexpression of miR-153-5p notably enhanced PTX sensitivity in MDA-MB-231/PTX xenograft model. Conclusion We found that overexpression of miR-153-5p could reverse PTX resistance in PTX-resistant TNBC cells via inducing G2/M phase arrest, indicating that miR‑153-5p may be a promising agent for patients with PTX-resistant TNBC.Gastric cancer is the third leading cause of malignant tumor-related mortality worldwide. Traditional cytotoxic agents prolong the overall survival and progression-free survival of patients with advanced gastric cancer (AGC) compared to that with best supportive care. Due to the occurrence of serious adverse drug reactions that result in discontinued treatment, the survival benefit in AGC remains unsatisfactory. Systemic chemotherapy regimens have changed greatly, especially since the introduction of trastuzumab. Nevertheless, HER2 positivity is present in only approximately 20% of tumors. Due to the genetic heterogeneity and complexity of patients, there are many studies in progress that are exploring novel targeted drugs as an alternative to chemotherapy or adjuvant treatment in early-stage, progressive, and advanced gastric cancer. On the basis of the differences in gene expression profiles among patients, searching for specific and sensitive predictive biomarkers is important for identifying patients who will benefit from a specific targeted drug. With the development of targeted therapies and available chemotherapeutic drugs, there is no doubt that, over time, more patients will achieve better survival outcomes. Recently, immune checkpoint blockade has been well developed as a promising anticancer strategy. This review outlines the currently available information on clinically tested molecular targeted drugs and immune checkpoint inhibitors for AGC to provide support for decision-making in clinical practice.Background Recent evidence showed cancerous inhibitor of protein phosphatase 2A (CIP2A) plays carcinogenesis roles in several types of human cancer. However, the expression and function of CIP2A in gliomas are unknown. Methods qRT-PCR, IHC and Western blot were used to evaluate CIP2A expression in glioma tissues and cell lines. The influence of CIP2A on prognosis was analyzed by KM curve and Cox regression. CCK8, clonal formation, transwell and tumor xenograft assays were used to analyze cell proliferation and invasion. The upstream microRNA of CIP2A was verified by luciferase and RIP assays. Results CIP2A was overexpressed in gliomas and associated with tumor size, WHO grade and postoperative overall survival rate. Depletion of CIP2A inhibited glioma cellular proliferation, invasion and xenograft tumorigenicity. miR-383 could bind to the 3'-UTR of CIP2A and inhibit CIP2A expression by forming an RNA-induced silencing complex with Ago2. Conclusion CIP2A plays a carcinogenesis role in glioma progression and is one of the potential targets of miR-383.Background Cisplatin (DDP) is the first-line chemotherapy agent for the treatment of oral squamous cell carcinoma (OSCC). The emergence of DDP resistance leads to diminished drug efficacy and survival benefit. lncRNA MALAT1 has been considered as one of the most important factors in OSCC. It has also been reported to enhance chemo-resistance in other kinds of carcinomas. However, little is known about the role of lncRNA MALAT1 in DDP resistance of OSCC. learn more Materials and methods Two kinds of human DDP-resistant cell lines (CAL-27R and SCC-9R) were developed from cisplatin-naïve cell lines (CAL-27 and SCC-9, respectively) as in vitro cell models. Cell transfection was performed to overexpress or knockdown MALAT1 in these cells. Mouse xenograft models were also established. The following measurements were performed cell proliferation, colony formation, wound healing, transwell, and TUNEL assays, as well as Western blot and immunofluorescence staining. Results DDP-resistant cells showed higher expression level of MALAT1 compared to cisplatin-naïve cells. The overexpression of MALAT1 in cisplatin-naïve cells enhanced DDP resistance and suppressed apoptosis in OSCC cells. However, the knockdown of MALAT1 in DDP-resistance cells induced apoptotic cell death and restored the sensitivity to DDP. Further analyses suggested that MALAT1 might promote DDP resistance via regulating P-glycoprotein expression, epithelial-mesenchymal transition process, and the activation of PI3K/AKT/m-TOR signaling pathway. Conclusion MALAT1 might be a potential therapeutic target for the treatment of DDP-resistant OSCC.Background Emerging evidence suggests that circular RNAs (circRNAs) are vital regulators in a range of cancers. "miRNA sponge" is the most reported role played by circRNAs in many tumors. The insulin-like growth factor (IGF) 1 pathway plays a key role in the development and progression of many cancers, including colorectal cancer (CRC). The aim of the study is to establish the potential clinical value and driving molecular mechanisms of circRNAs in CRC. Materials and methods Real-time quantitative RT-PCR (qRT-PCR) was performed to measure the circRUNX1 expression in 52 tissue samples from CRC patients. We verified the tumor promotor role of circRUNX1 in cell-based in vitro and in vivo assays. Human growth factor array was used to identify circRUNX1-regulated signaling pathways. We then used a double luciferase reporter assay and RNA fluorescence in situ hybridization to identify the downstream miR-145-5p of circRUNX1. Furthermore, we performed Western blotting and biological function assays to demonstrate if dicator and therapeutic target in CRC patients.Renal cell carcinoma (RCC) is among the 10 most common cancers in the USA. One-third of the patients diagnosed with this cancer present with locally advanced or metastatic disease. In the past, advanced disease conferred poor survival outcomes; however, the treatment paradigm for RCC has been revolutionized twice since 2005. The initial wave of revolution came with the emergence of vascular endothelial growth factor (VEGF) inhibitors and a second wave arose more recently with the emergence and unprecedented success of checkpoint inhibitors in RCC. A third wave combining these two strategies is well underway and likely represents the new paradigm to improve survival outcomes for afflicted patients. In this review, we discuss the current treatment landscape for patients with advanced RCC, focusing on approved VEGF and checkpoint inhibitors in the first-line setting as well as highlighting landmark combination clinical trials.[This corrects the article DOI 10.2147/OTT.S31387.].Purpose Exosomes participate in cellular communications by transmitting active molecules, including long noncoding RNAs (lncRNAs) and are regarded as suitable candidates for disease diagnosis. This study aimed to identify gastric cancer (GC)-specific exosomal lncRNA and investigate the potential diagnostic value of plasma exosomal lncRNA in GC. Patients and methods Exosomes from the culture media (CM) of four GC cells (GCCs) and human gastric epithelial cells were isolated. Exosomal RNA was extracted, and lncRNA microarray assay was performed to identify GC-specific exosomal lncRNAs. The expression levels of the candidate exosomal lncRNAs were validated in 120 subjects via quantitative reverse transcription PCR (qRT-PCR). The receiver operating characteristic (ROC) curve and area under curve were used to estimate the diagnostic capacity. We investigated the potential relationship between plasma exosomal lncRNA expression and the clinicopathological parameters of GC. Results A total of 199 exosomal lncRNAs were expressed at considerable higher levels in GCCs than those in normal controls, among which the top 10 upregulated lncRNAs were selected for further validation in cell, CM, and plasma.