Mahmoudmccaffrey1304
To detect the expression of long non-coding ribonucleic acid (lncRNA) NCK1-AS1 in non-small cell lung cancer (NSCLC), analyze the association between its expression and the clinicopathological characteristics of NSCLC patients, and study the biological function of NCK1-AS1 in vitro.
The relative expression of NCK1-AS1 in NSCLC tissues and cells was detected via quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The association between the expression of NCK1-AS1 and the clinicopathological characteristics of NSCLC was statistically analyzed. The effects of interference in the expression of NCK1-AS1 on the biological behaviors of NSCLC cells were detected via in vitro experiments, including Cell Counting Kit-8 (CCK-8) assay, colony formation assay and flow cytometry. After interference in the expression of NCK1-AS1, the expression of cyclin-dependent kinase 1 (CDK1) was determined using Western blotting.
The results of qRT-PCR showed that the expression of NCK1-AS1 was up-regulated in 50 out of 64 cases of NSCLC tissues. It was found via statistical analysis that highly expressed NCK1-AS1 was positively correlated with tumor size, TNM stage and lymph node metastasis. The results of qRT-PCR revealed that the expression of NCK1-AS1 was also up-regulated in NSCLC cells. After interference in the expression of NCK1-AS1, the proliferation of NSCLC cells was inhibited, and the cell cycle was arrested at G2/M phase. The results of Western blotting manifested that the expression of CDK1 was suppressed after interference in the expression of NCK1-AS1.
The expression of NCK1-AS1 is up-regulated in NSCLC, which indicates a poor prognosis. Highly expressed NCK1-AS1 promotes the proliferation of NSCLC cells through activating CDK1.
The expression of NCK1-AS1 is up-regulated in NSCLC, which indicates a poor prognosis. Highly expressed NCK1-AS1 promotes the proliferation of NSCLC cells through activating CDK1.
To investigate the relationship between the expression of receptor for advanced glycation end products (RAGE) and high-mobility group box-1 (HMGB1) and the clinical and pathological parameters and prognosis of the patients with gastric cancer (GC) with diabetes mellitus (DM).
30 normal gastric mucosa, 30 tissues with GC, 90 tissues with GC and DM and their clinical data were collected. The expression levels of RAGE and HMGB1 were detected by immunohistochemistry. Kaplan-Meier survival curve was used to analyze the relationship between the expression levels of RAGE and HMGB1 and the 5-year survival rate. MTT and cell scratch assays were used to detect the effects of knockdown RAGE and HMGB1 on the proliferation and migration of BGC-823 cells. Real-Time PCR was used to detect the regulation of RAGE and HMGB1 on PTBP-1, and Spearman correlation analysis was performed to analyze the correlation between RAGE and HMGB1 and Polyprimidine tract protein (PTBP-1).
Compared with the normal gastric mucosa group, thor the prognosis of patients with GC with DM. RAGE and HMGB1 may regulate the expression of PTBP-1 and inhibit the glycolysis of cells, which may affect the cell proliferation and migration of GC.
To detect the expression of high-mobility group nucleosome-binding domain 5 (HMGN5) in colorectal cancer tissues, to explore the function of HMGN5 on the proliferation and metastasis of colorectal cancer cells, and to further study the molecular mechanism of HMGN5 in the malignant progression of colorectal cancer (CRC).
The cancer tissues and para-carcinoma tissues were harvested from 40 patients with CRC. The expression of HMGN5 was detected via quantitative real-time polymerase chain reaction (qRT-PCR), and the relation between HMGN5 and clinical indexes of CRC patients was further analyzed. The CRC HT29 and HCT116 cell lines with high expression levels of HMGN5 were selected, and the HMGN5 knockdown model was established. The functions of HMGN5 on CRC cells were stated by cell counting kit-8 (CCK-8) assay and transwell migration assay. Then, the association between HMGN5 and fibroblast growth factor 12 (FGF12) was further explored via Dual-Luciferase reporter assay and reverse assay.
The qRT-PCR showetween HMGN5 and FGF12.
HMGN5 can increase the proliferative and migrative capacity of CRC cells via targeted binding to FGF12. In addition, clinical data analyses demonstrate that HMGN5 is intimately related to the incidence rate of lymph node metastasis and distant metastasis in patients with CRC.
HMGN5 can increase the proliferative and migrative capacity of CRC cells via targeted binding to FGF12. In addition, clinical data analyses demonstrate that HMGN5 is intimately related to the incidence rate of lymph node metastasis and distant metastasis in patients with CRC.
We aimed to determine the expression level of long intergenic non-coding ribonucleic acid 1605 (LINC01605) in colorectal cancer (CRC), and to explore the effects of the LINC01605/microRNA (miR)-3960/sex-determining region Y-box 11 (SOX11) regulatory axis on the biological behaviors of CRC cells and the molecular mechanism therein.
Tissue specimens were collected from 38 patients with CRC, and the relative expression level of LINC01605 in the CRC tissues and CRC cells was measured using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Then, the effects of LINC01605 on the proliferation, apoptosis, invasion and metastasis of CRC cells were observed via in vitro assays [cell counting kit (CCK)-8 assay, flow cytometry and transwell assay]. Besides, the possible miRNAs binding to LINC01605 were predicted by the bioinformatics method, and they were screened and verified using qRT-PCR and Dual-Luciferase reporter gene assay. Finally, the downstream target genes of miR-3960 were predicted bmigration and metastasis of CRC cells by the miR-3960/SOX11 regulatory axis.
LINC01605 has an up-regulated expression in CRC, and accelerates the proliferation, migration and metastasis of CRC cells by the miR-3960/SOX11 regulatory axis.
Kaempferol has been reported to play an anti-tumor role in various human cancers, while its role in gallbladder cancer (GBC) is unclear.
We found that kaempferol significantly inhibited the growth, invasion and migration, meanwhile induced apoptosis through cells arrested at G0/G1 phase of GBC cell lines, including GBC-SD and SGC996 cells in vitro.
Kaempferol promoted the release of cytochrome C from the mitochondria to cytoplasm, the activation of c-caspase-3 and c-caspase-9 and increased the expression levels of pro-apoptotic factor Bax, meanwhile decreased the expression levels of anti-apoptotic factor Bcl-2. In addition, the expression levels of CDK4, CDK6 and cyclin D1, which are members of the CDK4/CDK6/cyclin D1 signaling pathway, were also decreased by kaempferol. Moreover, kaempferol could efficiently prevent tumor progression of GBC in the xenograft in vivo.
Our results demonstrated that kaempferol suppressed GBC progression through activation of the CDK4/CDK6/cyclin D1 signaling pathway, suggesting that it might be a potential anti-tumor agent for clinical treatment of GBC.
Our results demonstrated that kaempferol suppressed GBC progression through activation of the CDK4/CDK6/cyclin D1 signaling pathway, suggesting that it might be a potential anti-tumor agent for clinical treatment of GBC.
The systemic immune-inflammation index (SII), an inexpensive and widely available hematologic marker of inflammation, has been linked to tumor progression, metastatic spread, and poor patient prognosis. The objective of this study is to explore the prognostic value of SII in patients with urinary system cancers (USCs).
A comprehensive literature search was conducted by searching the PubMed, EMBASE, Web of Science, Cochrane Library, Chinese National Knowledge Infrastructure (CNKI), and Wanfang databases from inception to May 10, 2020, to identify potential studies that assessed the prognostic role of the SII in USCs. The hazard ratio (HR) with a 95% confidence interval (CI) were used to evaluate the correlation between SII and overall survival (OS), progression-free survival (PFS), and cancer-specific survival (CSS) in USCs patients.
A total of 12 studies, including 2,693 USCs patients, were eventually included in the meta-analysis. Elevated SII index was significantly associated with poor OS (HR=1.28, 9nted to verify our findings.
Renal cell carcinoma (RCC) is one of the most common urological malignancies worldwide. Although great advances have been made in the diagnosis and management of RCC, its prognosis remains unsatisfactory. Long noncoding RNAs (lncRNAs) have been found to be essential factors in the initiation and development of cancer. The current study aimed to measure the expression and functions of lncRNA DNAJC3-AS1 in the progression of clear cell RCC (ccRCC).
The expression of lncRNA DNAJC3-AS1 was detected in 30 pairs of ccRCC tissues and in cell lines by RT-PCR, and its prognostic association with ccRCC was evaluated by the Kaplan-Meier method. The proliferation, migration, invasion and apoptosis of ccRCC cells were measured after silencing DNAJC3-AS1. The interaction between DNAJC3-AS1, miR-27a-3p and PRDM14 was identified by Dual-Luciferase reporter assay. The protein levels were measured by Western blotting.
The expression of DNAJC3-AS1 was upregulated in ccRCC tissues and cell lines compared to their normal counterparts. In vitro, silencing DNAJC3-AS1 reduced the proliferation, migration and invasion of ccRCC cells. Downregulation of DNAJC3-AS1 also led to the apoptosis of ccRCC cells. Moreover, we also found that DNAJC3-AS1 acted as a sponge of miR-27a-3p and identified PRDM14 as a target of miR-27a-3p.
LncRNA DNAJC3-AS1 acts as an oncogene and plays an essential role in the tumorigenesis of ccRCC, possibly via the regulation of the miR-27a-3p/PRDM14 axis.
LncRNA DNAJC3-AS1 acts as an oncogene and plays an essential role in the tumorigenesis of ccRCC, possibly via the regulation of the miR-27a-3p/PRDM14 axis.
CircRNAs have been proven to be vital during the process of malignant tumors. Their functions in bladder cancer (BCa) process remain largely unclear. This study aims to elucidate the role of circ0041103 in affecting the malignant phenotypes of BCa, and the possible molecular mechanism.
Circ0041103 expression levels in BCa tissues and cell lines were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The clinical significance of circ0041103 in influencing tumor size, tumor staging and lymphatic metastasis of BCa was analyzed. Regulatory effects of circ0041103 on proliferative and metastatic capacities of T24 and UM-UC-3 cells were examined through functional experiments. The binding target of circ0041103 and its downstream protein were predicted by online bioinformatic tools, which were further confirmed by Dual-Luciferase reporter assay and Pearson correlation test. The role of circ0041103/miR-107/ FOXK1 axis in regulating BCa process was explored by rescue experiments.
Circ0041103 was abnormally upregulated in BCa tissues and cell lines. click here Its level was higher in BCa tissues with a larger tumor size, or worse tumor staging, or BCa cases with lymphatic metastasis. Knockdown of circ0041103 inhibited proliferative and metastatic capacities of T24 and UM-UC-3 cells. MiR-107 was the binding target of circ0041103, and FOXK1 was the downstream gene of miR-107. Overexpression of circ0041103 could reverse the inhibited proliferative and metastatic capacities of T24 and UM-UC-3 cells overexpressing miR-107.
Circ0041103 is upregulated in BCa and predicts a poor prognosis in BCa. It stimulates BCa cells to proliferate and migrate via the miR-107/FOXK1 axis.
Circ0041103 is upregulated in BCa and predicts a poor prognosis in BCa. It stimulates BCa cells to proliferate and migrate via the miR-107/FOXK1 axis.
