Linc00239 Facilitates the Progress of Clear Cell Renal Cell Carcinoma via the miR-204-5p/RAB22A Axis.

Long intergenic non-coding RNA 239 (Linc00239) acts as an oncogene in colorectal cancer (CRC), esophageal squamous cell carcinoma, and acute myeloid leukemia cells. However, its role and regulatory mechanisms in clear cell renal cell carcinoma (ccRCC) remain unknown. We used StarBase and The Cancer Genome Atlas databases to evaluate Linc00239 expression and its effect on ccRCC. Furthermore, the function of Linc00239 in ccRCC proliferation and metastasis was analyzed using Cell Counting Kit-8 and Transwell assays following Linc00239 knockdown. Subsequently, the Linc00239-miRNA-mRNA regulatory associations were selected based on miRanda, miTarbase, and previous references, and their expression levels and binding relationship were further validated using quantitative real-time polymerase chain reaction, western blotting and dual-luciferase reporter gene assay. Additionally, we transfected a miRNA inhibitor to evaluate whether the miR-204-5p/RAB22A (Ras-related proteins in brain 22a) axis was involved in Linc00239 function. Linc00239 was elevated in ccRCC and correlated with poor prognosis. Linc00239 knockdown inhibited ccRCC progression. Additionally, Linc00239 inhibition elevated miR-204-5p expression and repressed RAB22A levels. Moreover, miR-204-5p inhibitors attenuated this inhibitory effect on proliferation, migration, invasion, and RAB22A level when Linc00239 was knocked down. Linc00239 promotes ccRCC proliferation and metastasis by elevating RAB22A expression through the adsorption of miR-204-5p, which provides a clue for the diagnosis and treatment of ccRCC.

Investigation of the Connection Schemes between Decks in 3D NAND Flash.

Dual-deck stacking technology is an effective solution for solving the contradiction between the demand for increasing storage layers and the challenge of the deep hole etching process in 3D NAND flash. The connection scheme between decks is a key technology for the dual-deck structure. It has become one of the necessary techniques for 3D NAND flash storage density improvement. This article mainly studies the impact of connection schemes between decks on cell reliability. Based on experimental data and simulation analysis, unfavorable effects were found as the gate channeling the breakdown and data retention characteristics of the top cells in the lower deck deteriorated due to the local electric field enhancement in the connection scheme without a poly-plug. This mainly contributed to the structural change of these cells within process impact. They will suffer secondary etching during the upper deck channel etching process due to alignment issues between the upper and lower decks. In another scheme with a poly-plug connection between decks, the saturation current of the channel decreased and the current variation increased. The fundamental cause of the current anomaly is that the Poly-plug has a certain shielding effect on channel inversion and the weak inversion region becomes a bottleneck for the channel current. The increase in variation is due to the shielding effect differences in the different structures of the poly-plug. Therefore, for the connection scheme without a poly-plug, the article proposes to improve device reliability by increasing the oxide thickness between decks and setting the top cells of the lower decks to be virtual cells. For the connection scheme with a poly-plug, the plug's N-type doping scheme is proposed to avoid the current dropping anomaly.

Silence of linc00023 inhibits pyroptosis and promotes cell proliferation via regulating p53.

OBJECTIVE: The objective of our study is to investigate the role and potential mechanism of linc00023 in the development of pyroptosis in clear cell renal cell carcinoma (ccRCC). METHODS: We assessed the expression of linc00023 in cells using qRT-PCR. Following linc00023 knockdown, we monitored cell proliferation and the pyroptosis marker using MTS, qRT-PCR, western blot analysis, and ELISA assays. Additionally, we performed RNA sequencing after linc00023 knockdown and validated the involvement of p53 using western blot analysis. Furthermore, we evaluated the potential mechanism by assessing cell proliferation and the expression of the pyroptosis marker after treatment with a p53 activator in linc00023-inhibited cells. RESULTS: Linc00023 expression was downregulated in ccRCC cells. Among them, ACHN cells exhibited higher linc00023 expression and were selected for further investigation. Knockdown of linc00023 resulted in increased cell proliferation and decreased pyroptosis. Furthermore, inhibition of linc00023 led to changes in the expression of numerous mRNAs, including p53. Importantly, the p53 activator ReACp53 reversed the effects of linc00023 knockdown on cell proliferation and pyroptosis. CONCLUSION: In conclusion, our findings suggested that linc00023 regulates pyroptosis in ccRCC by modulating p53 expression.

miR-5590-3p inhibits the proliferation and metastasis of renal cancer cells by targeting ROCK2 to inhibit proliferation, migration and invasion.

The present study aimed to clarify the role of microRNA (miR)-5590-3p in the progression of renal cell carcinoma (RCC) and investigate the underlying mechanisms. The expression levels of miR-5590-3p, Rho-associated protein kinase (ROCK)2 and ß-catenin in RCC cells were measured by reverse transcription-quantitative PCR and western blot analysis. Following overexpression of miR-5590-3p and ROCK2 by transfection of miR-5590-3p mimics and GV367-ROCK2, respectively, changes in the proliferation, migration and invasion of RCC cells were determined through colony-formation, wound-healing and Transwell assays, respectively. The direct binding interaction between miR-5590-3p and ROCK2, initially predicted using Targetscan, was validated by a dual-luciferase reporter assay. The results indicated that miR-5590-3p was downregulated in RCC. Overexpression of miR-5590-3p led to downregulation of ROCK2 and ß-catenin and inhibited the proliferation, migration and invasion of RCC cells. The dual-luciferase reporter assay confirmed the binding relationship between miR-5590-3p and ROCK2. Of note, overexpression of ROCK2 effectively reversed the regulatory effects of miR-5590-3p on RCC cells. In conclusion, miR-5590-3p inhibits the proliferation, migration and invasion of RCC cells by targeting ROCK2, which is a potential molecular biomarker and therapeutic target for RCC.

Nc886 promotes renal cancer cell drug-resistance by enhancing EMT through Rock2 phosphorylation-mediated ß-catenin nuclear translocation.

Drug resistance is a significant challenge in the present treatment regimens of renal cell carcinoma (RCC). Our previous study confirmed that nc886 functions as an oncogene in RCC. Nevertheless, the role and underlying mechanism of nc886 in RCC drug resistance are unclear. In the present study, Sunitinib and Everolimus treatment, respectively, downregulated nc886 expression in a dose-dependent manner in all four renal cancer cell lines. Nc886 overexpression in 786-O cells and ACHN cells significantly reduced the sensitivity of cancer cells to both Sunitinib and Everolimus treatment, respectively, by promoting cell viability and inhibiting cell apoptosis, whereas nc886 silencing increased cancer cell sensitivity. In renal cancer cell line with the highest drug-resistance, 786-O cells, Sunitinib, or Everolimus treatment enhanced the cellular EMT and was further enhanced by nc886 overexpression while attenuated by nc886 silencing. In 786-O cells, nc886 overexpression significantly promoted EMT, ROCK2 phosphorylation, and ß-catenin nucleus translocation under Sunitinib or Everolimus treatment. Moreover, ROCK2 silencing significantly reversed the effects of nc886 overexpression on EMT, ROCK2 phosphorylation, and ß-catenin nucleus translocation, as well as drug-resistant renal cancer cell viability and apoptosis. In conclusion, it was demonstrated that nc886 promotes renal cancer cell proliferation, migration, and invasion, as demonstrated previously. nc886 also promotes renal cancer cell drug-resistance to Sunitinib or Everolimus by promoting EMT through Rock2 phosphorylation-mediated nuclear translocation of ß-catenin.

Circular RNA circFLNA inhibits the development of bladder carcinoma through microRNA miR-216a-3p/BTG2 axis.

Recent studies have shown that circular RNA circFLNA is abnormally expressed in a variety of malignant tumors, but its role and mechanism in bladder carcinoma (BCa) are still unclear. The present paper aims to contribute to research on the effects and mechanism of circFLNA on the malignant phenotype of BCa. In this study, the expressions of circFLNA, miR-216a-3p and BTG2 in BCa and BCa cells (EJ, T24, 5637, TCC-SUP) were detected by qRT-PCR. EdU staining, colony formation, Transwell assay, wound healing assays, and sphere formation assay were used to measure the cell proliferation, viability, invasion, migration, and cell stemness of BCa cells after circFLNA overexpression. In addition, the correlation existed between miR-216a-3p and circFLNA or BTG2 was confirmed by Dual-Luciferase Reporter assay and RNA pull-down. Western blot was utilized to determine the expression of BTG2, MMP2, epithelial-mesenchymal transition (EMT)-related proteins (vimentin, E-cadherin) and stem cell-specific proteins (CD34, OCT4, SOX2). Our study confirmed that downregulated circFLNA and BTG2 expression and upregulated miR-216a-3p were found in both BCa tissues and cell lines. Meanwhile, upregulated circFLNA inhibited proliferation, invasion and migration, EMT and stemness of BCa cells. MiR-216a-3p was a target gene of circFLNA and could target BTG2. Further analysis finally demonstrated that circFLNA sponged miR-216a-3p and indirectly promoted BTG2 expression, ultimately regulating proliferation, migration, invasion and EMT of BCa cells. In conclusion, circFLNA inhibits the malignant phenotype of BCa cells and their stemness through miR-216a-3p/BTG2, thus suppressing BCa progression.

Endovascular removal of a misplaced ureteral stent in the vena cava: a complication of ultrasound-guided percutaneous nephrolithotomy.

Intravascular migration of a double J stent into the inferior vena cava is an uncommon complication. Active prevention, timely diagnosis, and early intervention are crucial for this complication. Intravascular interventional therapy is relatively easy, less traumatic, and has a high success rate. It can be used to select patients for intravascular ectopic DJS treatment.

Hydrogel Carbohydrate-Electrolyte Beverage Does Not Improve Glucose Availability, Substrate Oxidation, Gastrointestinal Symptoms or Exercise Performance, Compared With a Concentration and Nutrient-Matched Placebo.

The impact of a carbohydrate-electrolyte solution with sodium alginate and pectin for hydrogel formation (CES-HGel), was compared to a standard CES with otherwise matched ingredients (CES-Std), for blood glucose, substrate oxidation, gastrointestinal symptoms (GIS; nausea, belching, bloating, pain, regurgitation, flatulence, urge to defecate, and diarrhea), and exercise performance. Nine trained male endurance runners completed 3 hr of steady-state running (SS) at 60% V˙O2max, consuming 90 g/hr of carbohydrate from CES-HGel or CES-Std (53 g/hr maltodextrin, 37 g/hr fructose, 16% w/v solution) in a randomized crossover design, followed by an incremental time to exhaustion (TTE) test. Blood glucose and substrate oxidation were measured every 30 min during SS and oxidation throughout TTE. Breath hydrogen (H2) was measured every 30 min during exercise and every 15 min for 2 hr postexercise. GIS were recorded every 15 min throughout SS, immediately after and every 15-min post-TTE. No differences in blood glucose (incremental area under the curve [mean ± SD]: CES-HGel 1,100 ± 96 mmol·L-1·150 min-1 and CES-Std 1,076 ± 58 mmol·L-1·150 min-1; p = .266) were observed during SS. There were no differences in substrate oxidation during SS (carbohydrate: p = .650; fat: p = .765) or TTE (carbohydrate: p = .466; fat: p = .633) and no effect of trial on GIS incidence (100% in both trials) or severity (summative rating score: CES-HGel 29.1 ± 32.6 and CES-Std 34.8 ± 34.8; p = .262). Breath hydrogen was not different between trials (p = .347), nor was TTE performance (CES-HGel 722 ± 182 s and CES-Std: 756 ± 187 s; p = .08). In conclusion, sodium alginate and pectin added to a CES consumed during endurance running does not alter the blood glucose responses, carbohydrate malabsorption, substrate oxidation, GIS, or TTE beyond those of a CES with otherwise matched ingredients.

Long non-coding RNA CASC2 regulates Sprouty2 via functioning as a competing endogenous RNA for miR-183 to modulate the sensitivity of prostate cancer cells to docetaxel.

Prostate cancer (PC) is the most common cancer in men; however, limited effect is obtained due to the therapy resistance. CASC2 acts as a tumor suppressor in human malignancies serving as a ceRNA for miRNAs; Sprouty2 (SPRY2), a key antagonist of RTK signaling, also serves as a tumor suppressor. Herein, CASC2 and SPRY2 expression was down-regulated in PC tissues and cell lines; the overexpression of CASC2 and SPRY2 could suppress PC cell proliferation, promote PC cell apoptosis, and enhance the sensitivity of PC cells to docetaxel. CASC2 positively regulated SPRY2 expression and inhibited downstream extracellular regulated protein kinases (ERK) signaling activation through SPRY2. By using online tools, miR-183 might be a direct target of CASC2, and might simultaneously bind to the 3'UTR of SPRY2. The direct binding between CASC2, miR-183 and SPRY2 was then validated; miR-183 inhibition enhanced the cytotoxicity of docetaxel on PC cells, which could be partially attenuated by SPRY2 knockdown. In summary, CASC2 competes with SPRY2 for miR-183 binding to rescue the expression of SPRY2 in PC cells, thus enhancing the sensitivity of PC cells to docetaxel through SPRY2 downstream ERK signaling pathway; CASC2 and SPRY2 might be novel adjuvants for docetaxel-based chemotherapy for PC.

miR-27a in serum acts as biomarker for prostate cancer detection and promotes cell proliferation by targeting Sprouty2.

Prostate cancer (PCa) exhibits a high incidence among men, but there is no effective and non-invasive biomarker for the diagnosis of PCa, and the pathogenesis of PCa remains unclear. The present study identified that miR-27a was significantly overexpressed in the tumor tissues and sera of patients with PCa. In addition, high serum levels of miR-27a were correlated with poor survival in patients with PCa. Receiver-operating characteristic curves analysis demonstrated that the serum levels of miR-27a exhibited a high area under the curve value. Furthermore, miR-27a mimics or inhibitors significantly promoted or repressed the proliferation of PCa cells, respectively. In addition, it was identified that the expression of Sprouty2 (SPRY2) was inversely correlated with the expression of miR-27a in PCa tissues. The knockdown or overexpression of SPRY2 promoted or suppressed the proliferation of PCa cells, respectively, and the overexpression of SPRY2 inhibited the increased proliferation and cell cycle distribution of PCa cells mediated by miR-27a mimics. Taken together, these data indicated that the serum levels of miR-27a may be a novel and non-invasive biomarker for the diagnosis and prognosis of patients with PCa, and miR-27a/SPRY2 may be a therapeutic target for the treatment of PCa.

Interleukin-33 Predicts Poor Prognosis and Promotes Renal Cell Carcinoma Cell Growth Through its Receptor ST2 and the JNK Signaling Pathway.

BACKGROUND/AIMS: Renal cell carcinoma (RCC) is currently the ninth most common cancer in men. Interleukin (IL)-33 expression has previously been associated with a number of cancers; however, its biological role in RCC is poorly understood. In this study, we sought to elucidate the role of IL-33 in RCC. METHODS: Serum IL-33 levels were measured by ELISA. IL-33 expression in clinical RCC samples was examined by immunocytochemistry. The proliferation and apoptosis rate of RCC were determined by CCK8 and flow cytometry. Mcl1 and Bcl-2 expression were measured by quantitative real-time PCR and western blotting. JNK expression were measured by western blotting and flow cytometry. The in vivo role of IL-33 in RCC tumorigenesis was examined by animal models. RESULTS: We found that increased expression of IL-33 in RCC was associated with tumor-lymph node-metastasis (TNM) stage and inversely correlated with prognosis. IL-33 enhances RCC cell growth in vivo and stimulates RCC cell proliferation and prevents chemotherapy-induced tumor apoptosis in vitro. Furthermore, we demonstrated that IL-33 promotes RCC cell proliferation and chemotherapy resistance via its receptor ST2 and the JNK signaling activation in tumor cells. CONCLUSION: Our findings suggest that targeting IL-33/ST2 and JNK signaling may have potential value in the treatment of RCC.