Notes

Clippane: any routinely interlocked particle (MIM) determined by molecular tweezers.
mising therapeutic target for GC treatment. © 2020 He et al.Background Glioma is one of the most common malignant tumors. Glioblastoma (grade IV) is considered the most malignant form of human brain tumors. Maternal expression gene 3 (Meg3) encodes a non-coding RNA (ncRNA) that plays an important role in the development and progression of cancer. However, the role of Meg3 in glioma cells remains largely unclear. Methods Reverse transcription-quantitative (RT-q) PCR was conducted to evaluate the mRNA expression related to cell autophagy and EMT while protein expression was detected by Western blotting. Staining of acidic vacuoles and immunofluorescence staining were used to detect autophagy. The ability of cells to migrate and invade was detected by Transwell migration and invasion assays. Results In the present study, it was found that the overexpression of Meg3 induced EMT, migration and invasion of glioma cells, whereas Meg3 overexpression induced autophagy of glioma cells. More importantly, the inhibition of autophagy impaired the EMT of glioma cells. In addition, Meg3-induced EMT, migration and invasion could be partially reversed by autophagy inhibitors, chloroquine (CQ) and Lys05, in glioma cells. Conclusion All data suggest that Meg3 induces EMT and invasion of glioma cells via autophagy. Overall, the findings of the present study demonstrate the importance of Meg3 in the molecular etiology of glioma, which also indicate its potential applications in the treatment of glioma. © 2020 Yang et al.Background Hepatocellular carcinoma (HCC) is the third major cause of cancer-related death. Mounting evidence shows that microRNAs play critical roles in the initiation and progression of HCC and may potentially serve as diagnostic markers for HCC. Methods and Results In the present study, we explored the biological effects of miR-885-5p on HCC progression. We performed flow cytometry analyses of miR-885-5p in HCC cell lines and identified miR-885-5p as a recurrence-related microRNA. Overexpression of miR-885-5p significantly inhibited cell migration, invasion, proliferation, angiogenesis and EMT. Then, the correlation of miR-885-5p and AEG1 were confirmed by using luciferase assays, quantitative real-time PCR analysis and Western blotting. It was subsequently confirmed that Astrocyte Elevated Gene1 (AEG1) was a direct target gene of miR-885-5p. Conclusion miR-885-5p likely acts as a tumor suppressor by regulating AEG1, suggesting that miR-885-5p may be a potential biomarker and can be targeted in therapeutic strategies against HCC in the future. © 2020 Li et al.Liver cancer is a common malignant disease in China, while the primary hepatic neuroendocrine tumor (PHNET) is extremely rare presented with various manifestations. We herein describe an interesting PHNET case, which was clinically diagnosed as hepatocellular carcinoma (HCC) based on strong clinical evidence and the national guideline, but confirmed to be PHNET by pathology. A42-year-old Chinese male was admitted for persistent upper abdominal pain, and CT scan revealed a huge liver tumor in the left lobe. Proteinase K The tumor presented attributes of tumor rupture, portal vein tumor thrombus, elevated serum AFP level, background hepatitis B virus infection history, and radiological features mimicking typical HCC. After left semi-hepatectomy was performed for curative treatment of the primary "HCC", the pathology demonstrated the correct diagnosis be poorly differentiated neuroendocrine carcinoma (NEC). The immunohistochemistry assays showed positive neuroendocrine markers of CgA and Syn and negative HCC markers of Hep Par 1 and GPC3, ruling out concurrent HCC. This case and literature review suggest that in spite of rare incidence, PHNET should be considered as a possible diagnosis when lacking a confirmative pathology result, even when sufficient evidence of typical presentation exist to establish the clinical diagnosis of HCC. © 2020 Huang et al.Purpose Abelmoschus manihot (L.) Medik. (Malvaceae) derived Huangkui capsules (HKC) represent a traditional Chinese medicine that has been widely applied to the clinical therapy of kidney and inflammatory diseases. The present study aimed to determine the potential therapeutic effects and underlying mechanisms of the ingredients on Multiple Myeloma (MM), an incurable disease that exhibits malignant plasma cell clonal expansion in the bone marrow. Methods A 5TMM3VT syngeneic MM-prone model was established and treated with HKC. Murine pre-osteoblast MC3T3-E1 and pre-osteoclast Raw264.7 cells were treated with nine flavonoid compounds extracted from the flowers of Abelmoschus manihot. MC3T3-E1 and Raw264.7 cells were then examined by alizarin red staining and tartrate-resistant acid phosphatase activity staining, respectively. The proliferation of two human MM cells (ARP1, H929) was examined by performing an MTT assay following treatment with flavonoid compounds. Additionally, the cell cycle was analyzed via staolic pathways. Conclusion These results of the present study indicated that the bio-active ingredients of HKC exerted protective effects on MM mouse survival through promoting osteoblastogenesis and suppressing osteoclastogenesis, thus improving the bone marrow microenvironment to inhibit MM cell proliferation. © 2020 Hou et al.Purpose The purpose of the present study was to investigate the biological and clinical significance of GATA binding protein 3 (GATA3) in bladder cancer patients. Patients and Methods For the detection of the correlation between GATA3 expression and bladder cancer, we downloaded the mRNA expression data from the Cancer Genome Atlas (TCGA) database and conducted immunohistochemistry staining on formalin-fixed paraffin-embedded (FFPE) sample tissues. Then, bladder cancer cell lines were utilized to investigate the potential functions of GATA3 by cell apoptosis, proliferation and cycle assays. Results The mRNA data from TCGA database and bladder cancer cell lines suggested that GATA3 mRNA expression was significantly higher compared with normal tissues and cells. Conversely, the Western blot assay revealed that the expression of GATA3 was significantly lower in bladder cancer than normal urothelial cell line. Additionally, we found that over-expression of GATA3 was significantly associated with tumor subtype (P = 0.001 in TCGA; P = 0.004 in FFPE tissues), earlier clinical stage (P less then 0.001 in TCGA; P less then 0.001 in FFPE) and lower grade tumor (P = 0.057 in TCGA; P = 0.002 in FFPE). Kaplan-Meier analysis and multivariate Cox regression analysis indicated that age (P less then 0.001 in both cohort), clinical stage (P = 0.028 in TCGA; P = 0.011 in FFPE), recurrence (P less then 0.001) and low GATA3 in TCGA cohort (P = 0.035) but high GATA3 in FFPE cohort (P = 0.033) were independent risk factors for overall survival in patients. The assay to detect potential functions of GATA3 indicated that this biomarker could arrest the cell cycle of G2/M and S phase in T24 cells, and inhibit bladder cancer cells proliferation. Conclusion Collectively, our findings identified that GATA3 served as an important prognosis biomarker for bladder cancer patients. However, the mechanism of GATA3 in bladder cancer deserves further studies. © 2020 Wang et al.Purpose Our previous studies have shown that miR-195 is reduced in cervical cancer tissues, and that upregulation of miR-195 suppressed cervical cancer cell growth and induced a cell cycle block. In this study, we aimed to further elucidate the mechanism of action between miR-195-5p and Yes-associated protein 1 (YAP1) in the malignant progression of cervical cancer. Methods MiR-195-5p and YAP1 were detected using qRT-PCR in cervical cancer cells transfected with miR-195-5p mimics or inhibitor. Cell proliferation, migration, and invasion ability were detected using MTT, wound healing, and transwell invasion assays. Dual luciferase reporter assay, qRT-PCR, and Western blot analysis were used to demonstrate that YAP1 was a target of miR-195-5p. Results Our results showed that miR-195-5p is negatively correlated with YAP1 protein levels but not with mRNA expression. Moreover, upregulation of miR-195-5p by transient transfection with miR-195-5p mimics in HeLa and SiHa cells inhibited cell proliferation, migration ability, invasiveness, and the EMT. Conversely, miR-195-5p downregulation produced opposite results. In addition, multiple miRNA target prediction sites showed that YAP1 was a potential target gene; this was confirmed by dual luciferase assay. Rescue experiments further confirmed that YAP1 is involved in miR-195-5p-mediated inhibition of proliferation, migration ability, invasiveness, and the EMT of cervical cancer cells. Conclusion Taken together, our data suggest that miR-195-5p may act as a tumor suppressor which could provide a theoretical basis for cervical cancer patient targeted therapy. © 2020 Liu et al.Background Non-small cell lung cancer (NSCLC) is a great threat to human health and the biology of the NSCLC still remains largely unknown. Aberrantly expressed long non-coding RNA (lncRNA) Small nucleolar RNA host gene 6 (SNHG6) was involved in the tumorigenesis and progression of various cancers. The aim of this study is to investigate the roles of SNHG6 in NSCLC. Methods qRT-PCR and Western blot assays were applied to detect gene expressions. Cell proliferation and migration assays were used to analyze the gene functions. Luciferase reporter assay, RNA Immunoprecipitation assay and Chromatin immunoprecipitation assay were performed to investigate the molecular mechanism. Results We found that SNHG6 expression was significantly increased in NSCLC tissues and cell lines and its high expression was correlated with malignant features of NSCLC. In in vitro assays, knockdown of SNHG6 significantly depressed the proliferation vitality and migration activity of NSCLC cells. Research on mechanisms revealed that SNHG6 exerted its tumorigenesis role by promoting ETS1 expression via competitively binding with miR-944 and miR-181d-5p. We also demonstrated that ETS1 enhanced the expression of WIPF1 via binding to its promoter and SNHG6 could thereby regulate the expression of ETS1 target genes including WIPF1, MMP2 and MMP9. Conclusion Our study illustrates that SNHG6 is an oncogene in NSCLC and involved in NSCLC tumorigenesis by regulating ETS1 signaling via miR-944 and miR-181d-5p. © 2020 Geng et al.This paper presents an extremely rare case of testicular metastasis arising from renal pelvis carcinoma. The testicle is a rare site of clinically detectable tumor metastasis, originating rarely from upper tract urothelial carcinoma (UTUC). There are only two cases concerning UTUC metastasis to the testis available in the literature. In this report, we presented a patient who developed serial testicle, lung, liver and retroperitoneal lymph node metastasis from primary urothelial carcinoma of the renal pelvis within one year after surgery and chemotherapy. In conclusion, for patients with a history of UTUC who present with testicular symptoms, clinicians should be highly alert for the possibility of malignant involvement at this site. © 2020 Wu et al.Objective Breast cancer is one of the most common and serious types of cancer, with a particularly unfavorable prognosis. Although dysregulation of β-galactoside α 2,6-sialyltransferase 2 (ST6GAL2) has been observed in multiple cancers, the mechanism involved remains to be clarified. In this study, we focused on the potential function of ST6GAL2 in the regulation of breast cancer. Methods Flow cytometry and CCK-8 were used to measure markers of the cell cycle proliferation, adhesion, and invasion. Real-time PCR and immunohistochemistry analysis were used to detect the expression levels of ST6GAL2 in breast cancer tissues. Western blot was used to analyze the expression level of genes correlated with focal adhesion and metastasis pathways in breast cancer cells. Results ST6GAL2 expression levels were higher in breast cancer tissues as compared to healthy tissues. ST6GAL2 expression was associated with tumor stage, survival time, and estrogen receptor (ER)/progesterone receptor (PR)/human epidermal growth factor receptor 2 (HER2) status of breast cancer patients.
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