Background/aim: Hepatocellular carcinoma (HCC) is a particularly malignant form of cancer prevalent throughout the world; however, there is a pressing need for HCC biomarkers to facilitate prognosis and risk assessment.
Patients And Methods: This paper reports on the potential prognostic value of WNK lysine deficient protein kinase 1 (WNK1) in cases of HCC. We analyzed the expression of WNK1 at the mRNA level using omics data from the UALCAN database. We then verified our findings through the immunohistochemical (IHC) staining of various human cancer tissue as well as 59 HCC samples paired with corresponding normal tissues. The prognostic value of mRNA or protein expression by WNK1 was evaluated using the Kaplan-Meier method.
Results: Initial screening results revealed significantly higher WNK1 expression levels in HCC tissue compared to normal tissue. Verification using the paired HCC samples confirmed that the expression of WNK1 was indeed significantly higher in HCC tissue samples than in adjacent normal tissues. High WNK1 expression levels were significantly correlated with clinicopathological variables, including gender and histologic grade. Kaplan-Meier survival analysis revealed that high WNK1 expression levels were associated with poor HCC prognosis. Finally, univariate and multivariate analysis identified WNK1 as a prognostic factor for TNM stage in cases of HCC.
Conclusion: In summary, WNK1 is overexpressed at the mRNA and protein levels, and correlated with poor prognosis. Thus, WNK1 expression could potentially be used as a biomarker in HCC prognosis.
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http://dx.doi.org/10.21873/invivo.12081 | DOI Listing |
Life Sci
December 2024
Department of Pharmacology, Cardiac & Cerebral Vascular Research Center, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou 510080, China. Electronic address:
Aims: Impairment of nitric oxide (NO) production is a major cause of endothelial dysfunction and hypertension. ClC-5 Cl channel is abundantly expressed in the vascular endothelium. However, it remains unclear how it regulates endothelial function.
View Article and Find Full Text PDFAm J Physiol Renal Physiol
December 2024
Molecular Physiology Unit, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, and Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Tlalpan, Mexico City, 14080 Mexico.
The field of the with no lysine kinases (WNKs) regulation of the thiazide-sensitive NaCl cotransporter (NCC) began at the start of the century with the discovery that mutations in two members of the family, WNK1 and WNK4, resulted in a condition known as Familiar Hyperkalemic Hypertension (FHHt). Since FHHt is the mirror image of Gitelman's syndrome that is caused by inactivating mutations of the SLC12A3 gene encoding NCC, it was expected that WNKs modulated NCC activity and that the increased function of the cotransporter is the pathophysiological mechanism of FFHt. This turned out to be the case.
View Article and Find Full Text PDFNeural Regen Res
December 2024
Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China.
Recent evidence suggests that ferroptosis plays a crucial role in the occurrence and development of white matter lesions. However, the mechanisms and regulatory pathways involved in ferroptosis within white matter lesions remain unclear. Long non-coding RNAs (lncRNAs) have been shown to influence the occurrence and development of these lesions.
View Article and Find Full Text PDFJ Genet Eng Biotechnol
December 2024
Department of Laboratory Diagnosis, the Second Affiliated Hospital of Harbin Medical University, Harbin, China. Electronic address:
Sci Rep
December 2024
Biochemical Pharmacology,William Harvey Research Institute, Barts & The London Faculty of Medicine &Dentistry, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK.
Local haemodynamics control arterial homeostasis and dysfunction by generating wall shear stress (WSS) which regulates endothelial cell (EC) physiology. Here we use a zebrafish model to identify genes that regulate EC proliferation in response to flow. Suppression of blood flow in zebrafish embryos (by targeting cardiac troponin) reduced EC proliferation in the intersegmental vessels (ISVs) compared to controls exposed to flow.
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