Notes

A new Platform for you to Streamline Blended Testing Methods throughout Rosetta.
Background/Aims The effects of microRNA-423 on proliferation and drug resistance of breast cancer cells were explored, the downstream target genes of miR-423 and the targeted regulatory relationship between them were studied. Methods RT-qPCR was used to detect the expression of miR-423 in breast cancer tissues and cell lines, and the transfection efficiency of miR-423 inhibitory vector miR-423-inhibitor was constructed and verified. CCK-8 and colony formation assays were used to examine the effect of miR-423 on tumor cell proliferation. Target gene prediction and screening and luciferase reporter assay were used to verify downstream target genes of miR-432. The mRNA and protein expression of miR-423target gene ZFP36 was detected by RT-qPCR and Western blotting. Results The expression of miR-423 was significantly higher than that in normal tissues. Compared to the non-malignant mammary epithelial cell line MCF-10A, the expression of miR-423 was significantly raised in MCR-7 and MCF-7/ADR cells. ZFP36 was a downstream target gene of miR-423 and negatively correlated with the expression of miR-423 in breast cancer. The knockdown of miR-423 can significantly enhance the cytotoxicity of the drug, increase the apoptotic rate of MCF-7/ADR cells. miR-423 was capable of activating the Wnt/β-catenin signaling pathway leading to chemoresistance and proliferation, whereas overexpression of ZFP36 reduced drug resistance and proliferation. Conclusion miR-423 acted as an oncogene to promote tumor cell proliferation and migration. ZFP36 was a downstream target gene of miR-423, and miR-423 inhibited the expression of ZFP36 via Wnt/β-catenin signaling pathway of breast cancer cells. © 2020 Xia et al.Objective Long noncoding RNA small nucleolar RNA host gene 1 (SNHG1) has been reported to be aberrantly expressed and plays an important role in human cancers, including esophageal squamous cell cancer. However, the regulatory mechanism underlying SNHG1 in the progression of esophageal squamous cell cancer is poorly defined. Materials and Methods Fifty-three esophageal squamous cell cancer patients were recruited and overall survival was analyzed. EC9706 and KYSE150 cells were cultured for study in vitro. The expression levels of SNHG1, microRNA (miR)-204 and homeobox c8 (HOXC8) were detected by quantitative real-time polymerase chain reaction and Western blot. Cell cycle distribution, apoptosis, migration and invasion were determined by flow cytometry and transwell assays, respectively. The target interaction among SNHG1, miR-204 and HOXC8 was validated by luciferase reporter assay and RNA immunoprecipitation. CDDO-Im clinical trial Xenograft model was established to investigate the role of SNHG1 in vivo. Results High expression of SNHG1 was exhibited in esophageal squamous cell cancer and indicated poor outcomes of patients. SNHG1 silence led to cell cycle arrest at G0-G1 phase, inhibition of migration and invasion and increase of apoptosis. miR-204 was validated to sponge by SNHG1 and target HOXC8 in esophageal squamous cell cancer cells. miR-204 knockdown or HOXC8 restoration reversed the inhibitive role of SNHG1 silence in the progression of esophageal squamous cell cancer cells. Furthermore, inhibiting SNHG1 decreased xenograft tumor growth by regulating miR-204 and HOXC8. Conclusion SNHG1 knockdown suppresses migration and invasion but induces apoptosis of esophageal squamous cell cancer cells by increasing miR-204 and decreasing HOXC8. © 2020 Li et al.Purpose Circular RNA (circRNA) is involved in the development of various cancers. However, whether circRNA can inhibit the tumorigenesis of non-small cell lung cancer (NSCLC) is still unclear. We aimed to explore the epigenetic function of tumor-suppressive circRNA (hsa_circ_RNA_0011780) and its downstream regulatory factors in NSCLC. Patients and Methods Quantitative polymerase chain reaction (qPCR) was used to evaluate hsa_circ_11780 expression in NSCLC tissues and cell lines. The impact of high hsa_circ_11780 expression on overall survival in patients with NSCLC was tested using the Log rank test. The association between decreased hsa_circ_11780 expression and clinicopathological features in patients with NSCLC was analyzed using the Chi-squared test. In vitro cell proliferation and apoptosis were assayed using the cell counting kit-8 (CCK-8) and flow cytometry, respectively. Mice xenograft models were used to determine the tumor promoting effects of hsa_circ_11780 on NSCLC in vivo. The underlying regulatorkedly associated with the proliferation, migration, and invasion of NSCLC, resulting in decreased survival. These findings suggest that this regulatory axis may serve as a novel therapeutic target in NSCLC. © 2020 Liu et al.Objective Acetyl-11-keto-β-boswellic acid (AKBA) is a triterpenoid, which is the main component of boswellic acid from Boswellia Serrata, a medicinal plant that has shown immense potential in anti-cancer therapy. This study aims to explore the roles and molecular mechanisms of AKBA on cell behavior in non-small cell lung cancer (NSCLC) cells. Materials and Methods The effects of AKBA on the cell viability in A549, H460, H1299, and BEAS-2B cells were determined by the CCK-8 assay. The colony formation assay was used to identify the effects of AKBA on cell proliferation. Potential roles of AKBA in regulating the cell cycle, apoptosis, and autophagy in A549 were evaluated by flow cytometry, Western blotting, reverse transcription-polymerase chain reaction (PCR) and immunofluorescence (IF). Results AKBA reduced cell viability in A549, H460, H1299, and BEAS-2B. In A549 cells, AKBA suppressed the clone formation, arrested the cell cycle at the G0/G1 phase, induced cellular apoptosis. We found that AKBA suppressed the formation of autolysosome, and decreased the expression levels of Beclin-1, LC3A/B-I, and LC3A/B-II proteins. Furthermore, AKBA also inhibited the expression levels of PI3K/Akt signaling pathway proteins. Conclusion AKBA exerts the anti-cancer effects via cell cycle arrest, apoptosis induction, and autophagy suppression in NSCLC cells. This body of evidence supports the potential of AKBA as a promising drug in the treatment of NSCLC. © 2020 Lv et al.
Here's my website: https://www.selleckchem.com/products/cddo-im.html