Chaseyildirim7448

Colon cancer is a common malignant tumor of the digestive system. This project verified the negative role of protein tyrosine phosphatase (SHP-2) in the regulation of colon cancer and further clarified the key targets and molecular mechanisms in the regulation process.

The expression levels of SHP-2 in colon cancer tissues, adjacent tissues, normal colon cell lines, and cancer cell lines were detected via Quantitative Real-time PCR (qRT-PCR). The effect of SHP-2 on colon cancer cell function was verified using cell proliferation, Transwell, scratch, and apoptotic assays. CD81 was identified as the interaction protein of SHP-2 by immunoprecipitation.

The expression of SHP-2 was decreased in colorectal cancer compared with that in adjacent tissues. This expression was also decreased in colon cancer cells compared with that in intestinal epithelial cells. In addition, the tumor tissues of patients with metastatic colon cancer exhibited downregulated expression of SHP-2 compared with those of patients with in colon cancer and provided guidance for the diagnosis and prognosis assessment of colon cancer.Autophagy is a critical cellular process that generally protects cells and organisms from harsh environment, including limitations in adenosine triphosphate (ATP) availability or a lack of essential nutrients. Metabolic reprogramming, a hallmark of cancer, has recently gained interest in the area of cancer therapy. It is well known that cancer cells prefer to utilize glycolysis rather than oxidative phosphorylation (OXPHOS) as their major energy source to rapidly generate ATP even in aerobic environment called the Warburg effect. Both autophagy and glycolysis play essential roles in pathological processes of cancer. A mechanism of metabolic changes to drive tumor progression is its ability to regulate autophagy. This review will elucidate the role and the mechanism of glycolysis in regulating autophagy during tumor growth. Indeed, understanding how glycolysis can modulate cellular autophagy will enable more effective combinatorial therapeutic strategies.

Hepatocellular carcinoma (HCC) is one of the most common human malignant tumors. The prognosis of HCC patients is still unsatisfying. In this study, we performed the integrated bioinformatics analysis to identify potential biomarkers and biological pathways in HCC.

Gene expression profiles were obtained from the Gene Expression Omnibus database (GSE55048, GSE55758, and GSE56545) for the screening of the common differentially expressed genes (DEGs) between HCC tissues and matched non-tumor tissues. DEGs were subjected to Gene Ontology, KEGG pathway, and Reactome pathway analysis. ex229 molecular weight The hub genes were identified by using protein-protein interaction (PPI) network analysis. The hub genes in HCC were further subjected to overall survival analysis of HCC patients. The hub genes were further validated by in vitro functional assays.

A total of 544 common differentially expressed genes were screened from three datasets. Gene Ontology, KEGG and Reactome analysis results showed that DEGs are significantly associatedshowed that

and

silence attenuated cell proliferation, invasion, and migration, and promoted chemosensitivity of HCC cells.

and

may serve as potential biomarkers for predicting the worse prognosis of patients with HCC.

In conclusion, the present study performed the integrated bioinformatics analysis and showed that KIF14 and KIF23 silence attenuated cell proliferation, invasion, and migration, and promoted chemosensitivity of HCC cells. KIF14 and KIF23 may serve as potential biomarkers for predicting the worse prognosis of patients with HCC.

The aim of this study was to evaluate the prognosis effect of PD-L1 in combination with CD8

tumor-infiltrating lymphocyte (TIL) or HIF-1α in head and neck squamous cell carcinoma (HNSCC).

A total of 63 patients who underwent surgical resection were included in this study. The level of PD-L1, CD8

TIL, and HIF-1α was determined by immunohistochemical analysis. The survival of patients was evaluated by Kaplan-Meier analysis. The prognostic power of these parameters was evaluated by C-index.

We observed that the survival of patients, who had a high level of PD-L1 in tumor cells, was significantly shorter than those who had a low level of PD-L1. However, the survival of patients who had a high level of PD-L1 in tumor microenvironment was significantly longer than patients with a low level of PD-L1 in tumor microenvironment. In addition, high level of CD8

tumor-infiltrating lymphocyte or low level of HIF-1α level suggests a better prognosis. Moreover, we observed that PD-L1 in combination with CD8

tumor-infiltrating lymphocyte and HIF-1α could significantly improve the prognostic effect of current TNM stage.

The results of this study suggest that the level of PD-L1, CD8

TIL, and HIF-1α are useful prognostic biomarkers for patients with HNSCC. Incorporating these biomarkers into current TNM stage of HNSCC improve the discriminatory capability of TNM stage.

The results of this study suggest that the level of PD-L1, CD8+TIL, and HIF-1α are useful prognostic biomarkers for patients with HNSCC. Incorporating these biomarkers into current TNM stage of HNSCC improve the discriminatory capability of TNM stage.

F-FDG PET and

I scans are important in the detection of metastases from differentiated thyroid carcinoma (DTC). The relationship of FDG and radioiodine (RAI) metabolism in bone metastases (BMs) from DTC and its prognostic value on RAI treatment is not clear.

The retrospective study included DTC patients with BMs from two medical centers, who underwent

F-FDG PET/CT scans and RAI therapy. Therapeutic response was evaluated by serum thyroglobulin (Tg) levels and anatomical imaging changes.

The analyses were performed on 30 patients with 72 BMs. Forty-two (42/72, 58%) lesions displayed simultaneous

I and

F-FDG uptake. BMs with positive

F-FDG uptake had a less favorable response to RAI therapy in comparison to those with negative

F-FDG uptake (

= 0.018), even in

I-avid lesions (

= 0.033). Sixteen (53%) patients had disease progression with a median PFI of 26 months (range 3 to 89 months). Compared to those with

I-avid but non-FDG-avid BMs, patients presenting with

F-FDG-avid BMs had shorter PFI, whether with

I uptake (p = 0.