Kjerlee5945

Among 331 histologically examined lymph nodes we could detect one micrometastasis, which was correctly defined as SLN (1/22). There were no false-negative findings. No adverse reactions to ICG occurred.

Our first results are indicating the concept of SLN concerning OCSCC after the application of real-time NIR fluorescence endoscopy. However, this has to be verified by more extended studies.

Our first results are indicating the concept of SLN concerning OCSCC after the application of real-time NIR fluorescence endoscopy. However, this has to be verified by more extended studies.

To investigate the expression and potential mechanism of GALNT10 in gastric cancer (GC).

A total of 60 cases of GC tissues, as well as normal tissues were collected. The total RNA of GC specimens and cells were extracted by TRIzol method and the level of GALNT10 was examined by quantitative real-time polymerase chain reaction (qRT-PCR). read more In addition, the relationship between GALNT10 and clinical parameters and prognosis of GC patients was analyzed. Subsequently, Lentivirus was used to construct GALNT10 knockdown GC cell lines, and cell counting kit-8 (CCK-8) and transwell assays were applied to analyze the influence of GALNT10 on GC cell function. Bioinformatics and Luciferase assay was used to evaluate the relationship between GALNT10 and HOXD13. Furthermore, 5-fluorouracil (5-Fu)-resistant cells were used to detect the relationship between GALNT10 and 5-Fu sensitivity of GC cells.

qRT-PCR results revealed that GALNT10 level was markedly increased in tissues, as well as cell lines of GC. Statistical ana to be a new therapeutic target for diagnosis of 5-fluorouracil resistance in GC.

GALNT10 could regulate the proliferative and migration ability of GC cells and reduce the sensitivity to 5-Fu by enhancing the expression of HOXD13. Therefore, GALNT10 was expected to be a new therapeutic target for diagnosis of 5-fluorouracil resistance in GC.

To explore the role and potential mechanism of isochorismatase domain-containing 1 (ISOC1) in gastric cancer.

The expression levels of ISOC1 in gastric cancer (GC) tissues, as well as corresponding cell lines, was evaluated by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). A cell line stably expressing ISOC1 was constructed by vector construction and cell transfection, and the proliferation ability of the stably transfected cells was examined. Subsequently, the ISOC1 target database was screened, which suggested that CDK19 may be the potential target. The correlation between ISOC1 and CDK19 mRNA and protein expressions in clinical tissue specimens and cell lines was evaluated by qRT-PCR and Western blot, and the Luciferase reporter gene experiment was applied to verify the regulatory effect of ISOC1 on CDK19.

ISOC1 was shown to be markedly increased in GC tissues compared to adjacent cancer tissues by qRT-PCR. In addition, compared with patients with low ISOC1 expression, the pathological sfore, our study may provide new ideas for understanding the progression of GC.

Many studies have revealed that long non-coding RNAs (lncRNAs) are related to various cancers, including colorectal cancer (CRC). This study aims to explore the biological function of lncRNA PSMA3-AS1 in CRC progression.

The expression levels of PSMA3-AS1 and miR-4429 were assessed by RT-qPCR. CRC progression was explored by cell viability, migration, and invasion using CCK-8 and transwell assays. The interaction between PSMA3-AS1 and miR-4429 was verified by bioinformatics analysis, Dual-Luciferase assay, and RIP assay.

It was found that PSMA3-AS1 expression was increased and miR-4429 expression was decreased in CRC tissues and cells. In addition, PSMA3-AS1 interference markedly hindered the proliferation, migration, and invasion of CRC cells. MiR-4429 was a direct target of PSMA3-AS1, and the knockdown of PSMA3-AS1 significantly suppressed miR-4429 expression. The depletion of PSMA3-AS1 inhibited CRC progression, which was neutralized by miR-4429 inhibitor.

PSMA3-AS1 accelerated CRC progression by regulating miR-4429 expression, which could be used as a potential therapeutic target for CRC patients.

PSMA3-AS1 accelerated CRC progression by regulating miR-4429 expression, which could be used as a potential therapeutic target for CRC patients.

The purpose of this study was to explore the correlation between circRNA-100876 and the clinicopathological parameters of patients with colorectal cancer (Cc).

Quantitative real-time polymerase chain reaction (RT-qPCR) was applied to detect the circRNA-100876 expression in Cc tissues and cell lines. Overall survival analysis was carried out to explore the correlation between circRNA-100876 and the prognosis of Cc patients by Kaplan-Meier method and Log-rank method. Subsequently, Chi-square test was used to investigate the clinical significance of circRNA-100876 in the clinicopathological parameters of Cc patients. Moreover, the expression of circRNA-100876 was inhibited by small interfering RNAs (siRNAs) in loss-of-function assay. Finally, the invasion ability of Cc cells was determined by transwell assay.

The results of this study manifested that circRNA-100876 was abnormally overexpressed in Cc tissues and cell lines, and the high expression of circRNA-100876 was clearly associated with the Clinical stage, T classification and Lymph node metastasis of Cc patients. Besides, Cc patients with high expression worsened overall survival. In addition, it was demonstrated that the inhibition of circRNA-100876 reduced the invasion ability of Cc cells.

Acting as a tumor promoter, circRNA-100876 might be regarded as a new potential biomarker for the diagnosis and therapy of Cc.

Acting as a tumor promoter, circRNA-100876 might be regarded as a new potential biomarker for the diagnosis and therapy of Cc.

The purpose of this study was to explore the potential influences of circ_0005273 and its downstream target KLF12 on the progression of pancreatic cancer.

Relative levels of circ_0005273 and KLF12 in paired pancreatic cancer tissues and normal tissues were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Then, the differences in clinical indicators and prognosis (overall survival and progression-free survival) between pancreatic cancer patients expressing high and low levels of circ_0005273 were compared. After knockdown of circ_0005273 in AsPC-1 and CFPAC-1 cells, viability and migratory ability were assessed by cell counting kit-8 (CCK-8), transwell and wound healing assays. The regulatory effect of circ_0005273 on KLF12 was determined through Western blotting assay. Finally, the interaction between circ_0005273 and KLF12 was tested by dual-luciferase reporter assay.

It was found that circ_0005273 was upregulated in pancreatic cancer tissues than that in normal tissues. Besides, pancreatic cancer patients expressing a high level of circ_0005273 had higher incidence rates of lymphatic metastasis and distant metastasis, as well as poor prognosis.