Notes

Cryptosporidium spp., Giardia duodenalis along with Toxoplasma gondii detection throughout vegetables consumed throughout Marrakech, Morocco.
Parthenolide has been demonstrated to have anticancer effects against various types of cancer. However, the functional role of parthenolid has yet to be clearly reported in renal cell carcinoma (RCC). The aim of the present study was to investigate the effect of parthenolide in RCC 786‑O and ACHN cells. CCK‑8 and colony‑formation assays were used to observe the proliferation of RCC 786‑O and ACHN cells. Migration and invasion abilities were assessed through Transwell assays. The stem cell‑like properties of RCC cell lines were evaluated by mammosphere formation assay. Western blot analysis was used to investigate the metastasis and epithelial‑mesenchymal transition (EMT) induced by parthenolide on the expression levels of MMP2, MMP9, E‑cadherin, N‑cadherin, vimentin and snail. HSP inhibitor review The results revealed that when the cells were treated with various concentrations of parthenolide, the rate of proliferation and growth was decreased in 786‑O and ACHN cells. The number of invasive cells in a field was approximately 170, 90, 40 and 190, 150, 70 in 786‑O and ACHN cells with 0, 4 and 8 µM of parthenolide treatment. MMP‑2/‑9 expression (P less then 0.05) was inhibited by parthenolide. The protein levels of E‑cadherin were increased (P less then 0.05) and N‑cadherin, vimentin and snail were decreased (P less then 0.05) by parthenolide treatment. In addition, Parthenolide inhibited the expression of cancer stem cell markers and the PI3K/AKT pathway. The present study confirmed that parthenolide inhibited RCC cell proliferation and metastasis and suppressed the stem cell‑like properties of RCC cell lines, which could be a potential strategy to treat RCC. However, further molecular mechanisms of parthenolide in RCC should be observed and reported in the future.Pancreatic cancer is associated with an exceedingly poor prognosis, warranting the development of novel therapeutic strategies and discovery of prognostic predictors. Given that chemoresistance‑related molecules are reportedly associated with the poor prognosis of pancreatic cancer, the present study aimed to identify molecules that could be efficacious therapeutic targets for pancreatic cancer. First, 10 patient‑derived xenografts (PDXs) were established from patients with pancreatic cancer. Subsequently, after treating tumor tissue generated from the PDXs with standard drugs, next‑generation sequencing (NGS) was performed using these tissues. The results of NGS analysis and immunohistochemical analysis on 80 pancreatic cancer tissues revealed that human epididymis protein 4 (HE4) expression in the anticancer drug‑treated PDX group was higher than that in the untreated PDXs. In addition, chemoresistance ability was observed in tumor cell lines overexpressing HE4. Furthermore, Kaplan‑Meier analysis of tumor tissues from 80 patients with pancreatic cancer was performed and it was found that patients with a high HE4 expression level had a poor survival rate compared with those who had a low HE4 expression level. Multivariate analysis also indicated the high expression level of HE4 was an independent poor prognostic biomarker. Thus, it was concluded that high gene and protein expression levels of HE4 mediate chemoresistance and are independent prognostic factors for pancreatic cancer.Lung cancer is the most frequently diagnosed cancer and the leading cause of cancer‑associated mortality worldwide. In the present study, a novel molecular therapeutic target for lung cancer was investigated. The protein expression level of fidgetin‑like 1 (FIGNL1) in human lung cancer tissues was determined and its potential functions in the H1299 and A549 lung cancer cell lines was subsequently studied. In addition, the protein expression level of FIGNL1 in 109 lung cancer samples and corresponding para‑cancerous tissues was investigated, using immunohistochemical staining. RNA interference and overexpression of FIGNL1 was used to determine the role of FIGNL1 in regulating cell proliferation, and cDNA microarray analysis was performed to identify the potential regulatory pathways. Lastly, the potential role of FIGNL1 in regulating tumorigenesis in lungs and also the proliferation of lung cancer cells was investigated. Firstly, lung cancer tissues were found to express higher protein levels of FIGNL1 and was significantly associated with decreased cell proliferation, migration and invasion abilities, and enhanced cell death. Overexpression of FIGNL1 significantly promoted cell proliferation, including decreased arrest at the G1 phase of the cell cycle and apoptosis, as well as increased ability for fission and migration. These in vitro findings were consistent with the results of the cell‑line derived xenografts in BALB/c nude mice, where tumor growth was decreased when injected with cells transfected with shFIGNL1. Collectively, these results provide suggest that FIGNL1 is involved in cell growth and tumorigenesis.MicroRNA (miR)‑mediated mRNA and multiple signaling pathway dysregulations have been extensively implicated in several cancer types, including gliomas. Although previous studies have reported that miR‑301a acts as an oncogene, the underlying mechanisms of miR‑301a in the initiation and progression of glioma remain unknown. The present study aimed to investigate the involvement of miR‑301a‑mediated signaling pathway dysregulation in glioma. The results identified that miR‑301a was significantly upregulated in gliomas and was associated with a poor prognosis based on The Cancer Genome Atlas and Chinese Glioma Genome Atlas databases. Moreover, zinc and ring finger 3 (ZNRF3) exerted a critical role in the miR‑301a‑mediated effects on the malignant phenotype, such as by affecting proliferation and apoptosis. Mechanistically, the TOP/FOP luciferase assay, western blotting and immunofluorescence results demonstrated that miR‑301a knockdown inhibited the wnt/β‑catenin signaling pathway, at least partially via ZNRF3, while ZNRF3 was a direct functional target of miR‑301a, as indicated by luciferase reporter assay and western blot analysis. Furthermore, ZNRF3 could in turn repress miR‑301a expression, which was dependent on the wnt pathway. Collectively, the present study identified a novel miR‑301a/ZNRF3/wnt/β‑catenin signaling feedback loop that serves critical roles in glioma tumorigenesis, and that may represent a potential therapeutic target.
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