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Besides, we identified ncRNA pivot including FENDRR and miR-92a-3p as well as transcription factors pivot including SPI1, STAT5A which significantly regulated the dysfunction module.
This study can help reveal core dysfunction modules, potential regulatory factors, and driver genes for pancreatic cancer, enhancing the understanding of its pathogenesis and providing a reference for prediction with respect to the survival time of patients with this condition.
This study can help reveal core dysfunction modules, potential regulatory factors, and driver genes for pancreatic cancer, enhancing the understanding of its pathogenesis and providing a reference for prediction with respect to the survival time of patients with this condition.
Pancreatic cancer is a most lethal disease with low survival rates and therefore understanding its molecular level development for early diagnosis is key for designing improved therapeutic strategies. The long non-coding RNAs DANCR were reported as oncogenes, which are upregulated in many cancer types including pancreatic cancer. The role of DANCR and its correlation with tumour suppressor protein MLL3 expression are keen to understand different pathological stages of pancreatic cancer.
The role of long non-coding RNAs DANCR in correlation with MLL3 was studied using histology, in situ hybridization, immunohistochemistry and Western blotting. TM00314 strain of mutant mice in KRAS G12A and MPL gene were used since they are able to develop initial and advanced stage of pancreatic cancer after 3 and 5 months of growth.
The initial pancreatic cancer tissue showed low grade of dysplasia with diffusion of the solid nature of cells and in advanced stages giant cells and foci formation was observed. The expression of DANCR showed gradual upregulated expression as pancreatic cancer progressed. Bismuth subnitrate molecular weight However, the expression of MLL3 was upregulated in the initial pancreatic condition, but its expression was restricted in advanced stages of pancreatic cancer. Additionally, the signals for MLL3 RNA expression were more when compared with the context of protein expression.
The results show that MLL3 was overexpressed in the initial pancreatic cancer to restrict cancer progression and in which DANCR had no role in regulating MLL3 but in advanced stages it downregulated MLL3.
The results show that MLL3 was overexpressed in the initial pancreatic cancer to restrict cancer progression and in which DANCR had no role in regulating MLL3 but in advanced stages it downregulated MLL3.
Pancreatic cancer (PC) is a lethal disease of the alimentary system and is ranked 4th in cancer-related deaths in United States. PC has a poor prognosis and limited therapeutic options. The main purpose of the current study was to demonstrate the anticancer effects of the naturally occurring Baicalein flavone in human cisplatin-resistant pancreatic carcinoma cell line CAPAN-2.
Cell viability was examined via MTT cell proliferative assay. Mitochondrial-mediated apoptosis was examined through DAPI and annexin V/propidium iodide (PI) staining using fluorescence microscopy along with estimation of apoptosis-related protein expressions like caspase-3, Bax, Bcl-2 for which western blot was used. Next, wound-healing and transwell assays were performed to find out the effects of Baicalein on cell migration and invasion, respectively.
The results showed that Baicalein induced dose-dependent and selective anticancer effects in CAPAN-2 PC cancer cells with much less cytotoxicity to normal HTRET-HPNE cells. The antiproliferative effects of Baicalein were due to apoptosis induction as the number of apoptotic cells increased on increasing doses of the test molecule. Western blotting analysis revealed that the expressions of caspase-3 and Bcl-2 were decreased and Bax was increased. The test molecule also induced S-phase cell cycle arrest in PC cells with decreasing the cyclin-B1 expressions. Cell migration and invasion analysis revealed that Baicalein induced dose-dependent suppression in migration and invasion of CAPAN-2 PC cell line.
Baicalein is a potential anticancer agent against PC cells and can be considered for PC systemic therapy provided more toxicological and in vivo studies are carried out.
Baicalein is a potential anticancer agent against PC cells and can be considered for PC systemic therapy provided more toxicological and in vivo studies are carried out.
This study aimed to assess the effect of pretreatment albumin-bilirubin (ALBI) score on treatment outcomes in pancreatic cancer (PC) patients with liver metastasis at the time of diagnosis treated with chemotherapy (CT) in the first-line setting.
This was a retrospective study of 273 PC patients ≥18 years of age who had liver metastasis at the time of diagnosis and received CT in the first-line. ALBI score was calculated through the following formula; [(log10 bilirubin (μmol/L)×0.66)+[albumin(g/l)×-0.0852]. Patients were stratified into 3 categories based on the ALBI score as follows; grade IALBI ≤-2.60, grade II-2.60<ALBI≤-1.39, and grade IIIALBI>-1.39.
A total of 273 patients, [180 (65.9%) men and 93 (34.1%) women], were evaluated. The median age was 60 years. ALBI grade was I in 45 (16.4%) patients, II in 156 (57.1%) patients, and III in 72 (26.5%) patients. Based on the ALBI grade, median progression-free survival (mPFS) was 9 months in grade I patients, 6 months in grade II patients, and 4 months in grade III patients (p=0.002), with median overall survival (mOS) durations of 12 months vs. 8 months vs. 5 months, respectively (p<0.001). Multivariate analysis showed that ALBI grade II (HR,1.543) or III (HR,2.260) negatively affected survival.
A higher pretreatment ALBI grade is related to worse OS and PFS in PC patients with liver metastasis treated with a first-line CT, and therefore it can help predict the treatment outcomes in these patients.
A higher pretreatment ALBI grade is related to worse OS and PFS in PC patients with liver metastasis treated with a first-line CT, and therefore it can help predict the treatment outcomes in these patients.
To explore the biological function of micro ribonucleic acid (miR)-200a in cervical cancer (CC).
HeLa cells were transfected with miR-200a inhibitor or negative control (NC). Next, the effects of miR-200a down-regulation on the proliferation of CC cells were detected via methyl thiazolyl tetrazolium (MTT) assay and colony formation assay. Subsequently, flow cytometry was performed to determine the role of miR-200a in regulating the apoptosis of CC cells. Finally, Western blotting was conducted to detect the effects of miR-200a on the hypoxia-inducible factor 1-alpha (HIF-1α)/vascular endothelial growth factor (VEGF) signaling pathway.
RT-qPCR results confirmed that miR-200a was significantly down-regulated in HeLa cells transfected with miR-200a inhibitor compared with those transfected with NC (p<0.05). Besides, in comparison with cells in NC group, HeLa cells with down-regulated miR-200a showed weakened proliferation ability (p<0.05) and a remarkably decreased colony number (p<0.05). Moreover, flow cytometry results manifested that the down-regulation of the miR-200a expression level obviously promoted cell apoptosis (p<0.
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