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Ovarian cancer (OC) has the highest mortality among gynecological malignancies. Therefore, it is urgent to explore prognostic biomarkers to improve the survival of OC patients. One of the most prominent metabolic characteristics of cancer is effective glycolysis. Hexokinase 1 (HK1), as the first rate-limiting enzyme in glycolysis, is closely related to cancer progression. However, the role of HK1 in OC remains unclear.
The Cancer Genome Atlas (TCGA) database was used to detect the expression of
in OC patients. The chi-squared test was performed to examine the correlations between
and patients' clinical characteristics. Survival analyses were undertaken to determine the relationship between HK1 and patient survival, while the univariate/multivariate Cox model was used to evaluate the role of HK1 in patient prognosis. Gene Set Enrichment Analysis (GSEA) was performed to ascertain the related signaling pathways of HK1. RT-qPCR was implemented to validate the mRNA expression of
in OC cells. MTT was unt analysis and Western blotting showed that HK1 was involved in MAPK/ERK signaling.
may be a biomarker for the poor prognosis of OC patients and a potential therapeutic target.
HK1 may be a biomarker for the poor prognosis of OC patients and a potential therapeutic target.
The molecular mechanism of perineural invasion (PNI) in stage II colorectal cancer (CRC) remains not to be defined clearly. This study aims to identify the genomic aberrations related to PNI in stage II CRC.
Using array-based comparative genomic hybridization (array-CGH), primary tumor tissues and paracancerous normal tissues of stage II CRC with PNI and without PNI were analyzed. We identified genomic aberrations by using Genomic Workbench and MD-SeeGH and validated the aberrations of selected genes by real-time polymerase chain reaction (PCR). Gene ontology (GO) and pathway analysis were performed to determine the most likely biological effects of these genes.
The most frequent gains in stage II CRC were at 7q11.21-q11.22, 8p11.21, 8p12-p11.23, 8q11.1-q11.22, 13q12.13-q12.2, and 20q11.21-q11.23 and the most frequent losses were at 17p13.1-p12, 8p23.2, and 118q11.2-q23. Four high-level amplifications at 8p11.23-p11.22, 18q21.1, 19q11-q12, and 20q11.21-q13.32 and homozygous deletions at 20p12.1 were discovered in Stage II CRC. Gains at 7q11.21-q22.1, 16p11.2, 17q23.3-q25.3, 19p13.3-p12, and 20p13-p11.1, and losses at 11q11-q12.1, 11p15.5-p15.1, 18p11.21, and 18q21.1-q23 were more commonly found in patients with PNI by frequency plot comparison together with detailed genomic analysis. It is also observed that gains at 8q11.1-q24.3, 9q13-q34.3, and 13q12.3-q13.1, and losses at 8p23.3-p12, 17p13.3-p11.2, and 21q22.12 occurred more frequently in patients without PNI. Further validation showed that the expression of FLT1, FBXW7, FGFR1, SLC20A2 and SERPINI1 was significantly up-regulated in the NPNI group compared to the PNI group. GO and pathway analysis revealed some genes enriched in specific pathways.
These involved genomic changes in the PNI of stage II CRC may be useful to reveal the mechanisms underlying PNI and provide candidate biomarkers.
These involved genomic changes in the PNI of stage II CRC may be useful to reveal the mechanisms underlying PNI and provide candidate biomarkers.
SPARC (secreted protein acidic and rich in cysteine), also known as osteonectin, BM-40, and 43 K protein, is a matricellular protein associated with various tumor progressions. The aim of this research was to investigate the prognostic value of SPARC in endometrial carcinoma (EC) and its function in cancer cell invasion and metastasis.
From both mRNA and protein levels, SPARC expression in normal endometrial tissue and EC tissue, normal endometrial cells and 4 EC cell lines (KLE, HEC-1A, HEC-1B, Ishikawa) were evaluated by immunohistochemistry (IHC) or immunocytochemistry (ICC), quantitative real-time PCR (qRT-PCR) and Western blotting. RNA interference mediated by lentivirus was performed to get the stable SPARC down-expressing cells. The functional analysis techniques in vitro and in vivo were used to detect the effects of SPARC knockdown on EC cell proliferation, apoptosis, invasion and metastasis.
The expressions of SPARC in EC tissues and cells were much lower than those in normal endometrial cells and tissues; meanwhile, its low expression was closely related to the malignant clinicopathological characteristics of EC. SPARC knockdown could inhibit apoptosis, promote the process of EMT and improve the proliferation and invasion capacities of EC cells in vitro and in vivo.
The low expression of SPARC was detected in EC tissues and cells, which was positively correlated with the poor prognosis of EC patients. SPARC acted as a tumor suppressor gene that hindered EC progression, which proposed a new therapeutic strategy for EC treatment.
The low expression of SPARC was detected in EC tissues and cells, which was positively correlated with the poor prognosis of EC patients. click here SPARC acted as a tumor suppressor gene that hindered EC progression, which proposed a new therapeutic strategy for EC treatment.
This study aimed at probing into the effect of long non-coding RNA (lncRNA) C-terminal binding protein 1 antisense RNA 2 (CTBP1-AS2) on gastric cancer (GC) cell proliferation and apoptosis, and its regulatory function on miR-139-3p and
.
Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to examine the expressions of CTBP1-AS2, miR-139-3p and
mRNA in GC cell lines and clinical specimens. Cell counting kit-8 (CCK-8) assay, flow cytometry and EdU assay were conducted to examine the effects of CTBP1-AS2 and miR-139-3p on GC cell proliferation and apoptosis. Western blot was applied for detecting the expressions of Bax, Bcl-2 and
. A lung metastasis mouse model was used to evaluate metastasis of GC cells in vivo. Bioinformatics, dual-luciferase report assay, RIP and RNA pull-down assays were utilized to validate the targeted relationship between CTBP1-AS2 and miR-139-3p as well as the targeting relationship between miR-139-3p and
.
CTBP1-AS2 was highly expressed in GC, and its high expression was strongly associated with increased TNM stage, increased tumor size and low degree of differentiation of the tumor tissues.
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