Beanerichsen2971
Cervical cancer is a fatal burden for women. Circular RNAs (circRNAs) are important regulators in cancer development. Our study aimed to investigate the function and action mechanism of a novel circRNA, circ_0084927, in cervical cancer.
The expression of circ_0084927, miR-142-3p and ADP-ribosylation factor-like protein 2 (ARL2) mRNA was measured by quantitative real-time polymerase chain reaction (qRT-PCR). For functional analyses, cell proliferation was assessed using cell counting kit-8 (CCK-8) assay. Cell cycle distribution was monitored by flow cytometry assay. Cell migration and cell invasion were evaluated by transwell assay. The interaction between miR-142-3p and circ_0084927 or ARL2 was predicted by the bioinformatics analysis and validated by dual-luciferase reporter assay and RNA immunoprecipitation assay (RIP) assay. The expression of ARL2 at the protein level was detected by Western blot. Animal tumor formation assay was performed to monitor the tumorigenicity of circ_0084927 in vivo.
The expression of circ_0084927 and ARL2 was enhanced in cervical cancer tissues and cells, while the expression of miR-142-3p was opposite to them. Circ_0084927 knockdown significantly blocked cervical cancer cell proliferation, migration and invasion and induced cell cycle arrest. MiR-142-3p was targeted by circ_0084927, and miR-142-3p inhibition reversed the effects of circ_0084927 knockdown. Besides, miR-142-3p bound to ARL2, and the inhibitory effects of miR-142-3p restoration on cell proliferation, cycle, migration and invasion were counteracted by ARL2 overexpression. check details , circ_0084927 upregulated ARL2 expression by sponging miR-142-3p. Circ_0084927 knockdown retarded tumor growth in vivo by regulating miR-142-3p and ARL2.
Circ_0084927 accelerated the progression of cervical cancer partly by mediating the miR-142-3p/ARL2 axis.
Circ_0084927 accelerated the progression of cervical cancer partly by mediating the miR-142-3p/ARL2 axis.
This study aimed to predict and explore the possible clinical value and mechanism of genetic markers in prostate cancer (PCa) using a bioinformatics analysis method.
The RNA-seq data were downloaded from The Cancer Genome Atlas (TCGA) database to identify the differentially expressed genes (DEGs). The hub genes were screened by building protein-protein interaction (PPI) subnetworks with four topological analysis methods. The overall survival analysis of hub genes was conducted using Kaplan-Meier curves. Furthermore, the bioinformatics results were confirmed in 102 PCa samples collected in our hospital. Gene Set Enrichment Analysis (GSEA) was performed to provide information about the molecular mechanisms underlying PCa.
Among 13 hub genes, the high expression of GTSE1 or KIF18B was associated with worse overall survival according to the TCGA samples. Immunoreactive scores for GTSE1 staining were significantly higher in PCa tissues than in paracancerous tissues (P<0.01). The overall survival time of patients with high GTSE1 expression was shorter than that of patients with low GTSE1 expression (P=0.015). GSEA demonstrated that high GTSE1 expression was mainly enriched in the cell cycle (P<0.001), DNA replication (P<0.001), mismatch repair (P<0.001), and p53 signaling pathway (P<0.001).
GTSE1 expression was significantly high in PCa and associated with poor prognosis. GTSE1 may serve as a potential biomarker and therapeutic target in PCa patients.
GTSE1 expression was significantly high in PCa and associated with poor prognosis. GTSE1 may serve as a potential biomarker and therapeutic target in PCa patients.
Breast cancer is one of the most common cancers worldwide. Long non-coding RNAs and microRNAs act as important regulators in human cancers. This study aims to explore the molecular mechanism among H19, miR-491-5p and zinc finger 703 (ZNF703) in breast cancer.
Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to detect the expression of H19, miR-491-5p and ZNF703. #link# Cell Counting Kit 8 (CCK-8) assay was performed to evaluate cell proliferation. Cell apoptosis was assessed by flow cytometry assay. The number of migrated and invaded cells was counted by transwell assay. Dual luciferase reporter assay was carried out to test luciferase activity. Protein level of ZNF703 was measured by Western blot assay.
H19 was highly expressed in breast tissues and cells. H19 knockdown inhibited proliferation, induced apoptosis and blocked migration and invasion. Moreover, H19 bound to miR-491-5p and negatively regulated miR-491-5p expression. MiR-491-5p inhibition abrogated the activities of proliferation, apoptosis, migration and invasion affected by H19 knockdown. Furthermore, miR-491-5p directly targeted ZNF703 and inversely modulated ZNF703 expression. ZNF703 up-regulation rescued the effects of miR-491-5p overexpression on proliferation, apoptosis, migration and invasion. In addition, H19 knockdown reduced ZNF703 expression by targeting miR-491-5p/ZNF703 axis.
H19 promoted proliferation, migration and invasion and retarded apoptosis of breast cancer cells via sponging miR-491-5p to down-regulate ZNF703 expression.
H19 promoted proliferation, migration and invasion and retarded apoptosis of breast cancer cells via sponging miR-491-5p to down-regulate ZNF703 expression.
Papillary thyroid carcinoma (PTC) has increased rapidly over recent years, and radiation, hormone effects, gene mutations, and others were viewed as closely related. However, the molecular mechanisms of PTC have not been cleared. Therefore, we intended to screen more accurate key genes and pathways of PTC by combining RT
profiler PCR arrays and bioinformatics methods in this study.
RT
profiler PCR arrays were firstly analyzed to identify differential expression genes (DEGs) in PTC. RT-qPCR were performed to verify the most significant differential expression genes. The TCGA database was used to further verify for expanded data. Enrichment analysis of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) was analyzed. To construct the protein-protein interaction (PPI) network, we used STRING and Cytoscape to make module analysis of these DEGs.
Sixteen differentially expressed genes were presented in RT
profiler PCR arrays, including 13 down-regulated DEGs (DEGs) and three up-regulated DEGs (DEGs), while 13 stable DEGs were eventually verified. A total of 155 DEGs were presented in the TCGA database, including 82 up-regulated DEGs (DEGs) and 73 down-regulated DEGs (dDEGs). A total of 29 important genes were extracted after integrating these two results, GO and KEGG analyses were used to observe the possible mechanisms of action of these DEGs. The PPI network was constructed to observe hub genes. Prognostic analysis further demonstrated the involvement of these genes in the biological processes of PTC.
This study identified some potential molecular targets and signal pathways, which might help us raise our awareness of the mechanisms of PTC.
This study identified some potential molecular targets and signal pathways, which might help us raise our awareness of the mechanisms of PTC.
Gastric cancer (GC) is a major cancer-related mortality disease. Gambogic acid (GA) has been investigated to inhibit cancer progression. In the present study, the molecular mechanism of GA in regulating GC progression was studied.
The expression levels of circular RNA ASAP2 (circ_ASAP2), miR-33a-5p and cyclin-dependent kinases 7 (
) were detected by quantitative real-time polymerase reaction (qRT-PCR).
protein level was evaluated by Western blot. link2 Cell colony formation assay, 3-(4,5-Dimethylthazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, transwell assay and flow cytometry analysis were employed to reveal the functional effects among circ_ASAP2, miR-33a-5p and
on GA-induced GC progression. Mechanistically, the binding relationship between miR-33a-5p and circ_ASAP2 or
was predicted with starBase v3.0 online database and verified by dual-luciferase reporter assay. In vivo tumor formation assay was used to explain the impacts of GA treatment on GC growth in vivo.
Circ_ASAP2 and
expressis by upregulating CDK7 expression through binding to miR-33a-5p in GA-induced GC cells. This study provided a theoretical basis in GC treatment with GA.
Due to the low rate of regional recurrence (RR) in early-stage breast cancer with pT1-2 and negative sentinel lymph node biopsy (SLNB), no regional therapy is suggested for them. link3 However, whether there is a subset of patients who were with high risk of regional failure and may benefit from regional treatment is still unknown. The current study was designed to identify the patients with high risk of RR, thereby providing clues for enhanced regional therapy.
We analyzed a total of 1124 breast cancer patients with pT1-2N0 from May 2004 to Dec 2014. All the patients were treated with breast-conservation surgery (BCS) and adjuvant whole-breast radiotherapy. The regional recurrence-free survival (RRFS), local regional recurrence-free survival (LRRFS), disease-free survival (DFS) and overall survival (OS) were assessed by using the Kaplan-Meier method. Cox proportional hazards regression was performed to detect factors in predicting the RRFS.
In multivariable analysis, both T stage and molecular type were significant predictors of RRFS. Patients with T2 stage had a lower RRFS than those with T1stage. Triple-negative patients were more likely to suffer regional failure than the patients with other molecular types. The two predictors were then employed to divide all the patients into three groups based on the risk level of RR. Patients with both T2 and triple-negative molecular type had the lower RRFS, LRRFS, DFS and OS than the patients with one or no risk factor.
For early-stage breast cancer patients with negative SLNB, those who were with both T2 stage and triple-negative molecular type had a high rate of RR and enhance regional therapy may be needed for them.
For early-stage breast cancer patients with negative SLNB, those who were with both T2 stage and triple-negative molecular type had a high rate of RR and enhance regional therapy may be needed for them.
Laryngeal cancer (LCA) is a common head and neck cancer. Lysine demethylase 5B (
) knockdown is expected as a new target for cancer prevention. We investigated the molecular mechanism of
in LCA.
The levels of
, microRNA
and high-mobility-group box 2 (
) in LCA tissues and cells, normal tissues and cells were detected. The effect of
on LCA was evaluated. The upstream miR of
and the downstream gene and pathway of
were predicted and their effects on LCA were analyzed. The Wnt/β-catenin pathway-specific activator agonist was delivered into LCA cells expressing
mimic to evaluate the role of the Wnt/β-catenin pathway.
was highly expressed in LCA, and inhibition of
suppressed LCA progression.
, downregulated in LCA tissues, was a regulatory miR of
. Overexpression of
significantly inhibited the malignant biological behaviors of LCA cells.
promoted
expression via histone demethylation.
was highly expressed in LCA, and overexpression of
promoted LCA progression by inducing the Wnt/β-catenin pathway.
