Notes

Design of a digital-PCR analysis to be able to measure fragmented human mitochondrial Genetics.
Previous studies have shown that non-SMC condensin I complex subunit G (
) overexpression is correlated to poor prognosis of multiple cancer types. Herein, we explored the underlying mechanism of
-mediated cardia adenocarcinoma (CA) proliferation and cell cycle regulation.

The protein profiling technology was used to analyze the gene expression in 20 CA and adjacent tissue samples. Differential genes were identified by bioinformatic analysis. Western blot and qRT-PCR-based analysis assessed the
expression levels in multiple CA cell lines. CA cell lines, SGC-7901 and AGS, were transfected with Lip 2000, and stably transfected cell lines were screened for
overexpression and downregulation. MTT and clone formation assays were employed to detect cell proliferation, and cell cycle phases were analyzed using flow cytometry. Western blot was performed to determine the
gene expression levels. Finally, we studied the tumorigenic effects of
in the mouse model and validated the cell experiment resultshrough PI3K/AKT signaling pathway activation.
The aberrantly expressed circular RNAs (circRNAs) are implicated in the progression of hepatocellular carcinoma (HCC). CircRNA hsa_circ_0006916 (circ_0006916) is dysregulated in HCC, but the function and mechanism of this circRNA in HCC development remain uncertain.

Thirty paired HCC and normal tissues were collected. circ_0006916, microRNA (miR)-599 and serine/arginine rich splicing factor 2 (
) abundances were examined via quantitative reverse transcription polymerase chain reaction or Western blot. Cell viability, colony ability, migration, invasion, cell cycle and apoptosis were tested via cell counting kit-8, colony formation, wound healing analysis, transwell analysis, and flow cytometry. The interaction between miR-599 and circ_0006916 or
was analyzed via dual-luciferase reporter and RNA immunoprecipitation analyses. The function of circ_0006916 on cell growth in vivo was analyzed via xenograft model.

circ_0006916 expression was increased in HCC tissues and cell lines. circ_0006916 knockdown reduced cell viability, colony formation, migration and invasion and caused cell cycle arrest and apoptosis. learn more miR-599 was targeted via circ_0006916, and miR-599 knockdown reversed the influence of circ_0006916 silence on HCC progression.
was targeted via miR-599, and miR-599 overexpression suppressed cell viability, colony formation, migration and invasion and promoted cell cycle arrest and apoptosis via decreasing
. circ_0006916 could regulate
expression via miR-599. circ_0006916 knockdown decreased HCC cell growth in the xenograft model.

circ_0006916 knockdown represses the progression of HCC via regulating miR-599 and
.
circ_0006916 knockdown represses the progression of HCC via regulating miR-599 and SRSF2.
Prostate cancer (PCa) is one of the most common malignant cancer in males worldwide. Circular RNAs (CircRNAs) are novel type of non-coding RNAs. Recently, circRNAs have been reported participating in various cancers, including prostate cancer. However, the function and mechanism of circ_0057553 remain to be elucidated.

The RNA expression levels of circ_0057553, miR-515-5p, YES proto-oncogene 1 (YES1) and glycolytic genes mRNA were detected by qRT-PCR in PCa tissues or cells. Western blotting was performed to analyze YES1 protein level. Cell viability, migration and invasion and cell apoptosis were assessed by cell counting kit-8 (CCK-8) assay, transwell assay and flow cytometry. In addition, the effects of cell glycolysis were evaluated by measuring lactate production, glucose consumption and adenosine triphosphate (ATP) level. Moreover, dual-luciferase reporter assay was used to detect the target sites of circ_0057553 and miR-515-5p, miR-515-5p and YES1. RNA immunoprecipitation (RIP) was conducted to evaluate the target relationship between circ_0057553 and miR-515-5p. Xenograft mouse model was conducted to measure tumor formation in vivo.

Circ_0057553 was significantly up-regulated in PCa tissues and cells. Knockdown of circ_0057553 inhibited cell viability, migration, invasion and glycolysis and facilitated apoptosis in PCa cells. Furthermore, circ_0057553 bound to miR-515-5p and miR-515-5p directly targeted YES1. Interestingly, miR-515-5p inhibitor partially rescued the function of circ_0057553 knockdown, while YES1 restored the effects of miR-515-5p overexpression. Circ_0057553 down-regulation remarkably decreased tumor volume and weight in vivo.

Circ_0057553 affected PCa cell viability, migration, invasion, apoptosis and glycolysis through miR-515-5p/YES1 axis.
Circ_0057553 affected PCa cell viability, migration, invasion, apoptosis and glycolysis through miR-515-5p/YES1 axis.
Bladder cancer (BC) is the most commonly occurring malignant tumor of the urinary system worldwide. Long non-coding RNAs (lncRNAs), including lncRNA RNF144A-AS1 (RNF144A-AS1), perform an oncogenic role in BC progression. However, how RNF144A-AS1 is regulated in BC has not been fully investigated, and its role in BC is mostly obscure. In this study, we explore its role in BC progression.

The expression level of RNF144A-AS1 in BC tissues was explored via bioinformatics analysis and quantitative real-time PCR (qRT-PCR). We used RNF144A-AS1 siRNA (si-RNF144A-AS1) to inhibit the RNF144A-AS1 level in BC cell lines (J82 and 5637 cells). A series of experimental studies in vitro (CCK-8 assay, colony formation assay and Transwell assay) was performed to explore the role of si-RNF144A-AS1 on the proliferation, migration and invasion of J82 and 5637 cells. A BC xenograft model was established, and the effect of si-RNF144A-AS1 on xenograft growth was explored in vivo. The interactions among RNF144A-AS1, miR-455-5p anthe critical role of RNF144A-AS1 in BC development, and our study reveals for the first time that RNF144A-AS1 promotes BC progression via the RNF144A-AS1/miR-455-5p/SOX11 axis.
Overall, our findings underline the critical role of RNF144A-AS1 in BC development, and our study reveals for the first time that RNF144A-AS1 promotes BC progression via the RNF144A-AS1/miR-455-5p/SOX11 axis.
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