Publications by authors named "Charles Shing Kam"
Article Synopsis
- Metabolic reprogramming in cancer is closely linked to hypoxia, which aids rapid tumor growth and reduces oxidative stress; PFKFB, a key glycolytic enzyme, is vital in various cancers but its role in hepatocellular carcinoma (HCC) is not well-studied.
- The researchers analyzed PFKFB4 expression using RNA sequencing and confirmed its up-regulation in HCC through various methods, discovering a correlation with certain genetic mutations and aggressive tumor behavior.
- Functional studies using CRISPR/Cas9 to knock out PFKFB4 demonstrated that its loss impaired HCC development and altered metabolite levels, affecting pathways like glycolysis and the pentose phosphate pathway.
Background And Aims: Ras-like (Ral) small guanosine triphosphatases (GTPases), RalA and RalB, are proto-oncogenes directly downstream of Ras and cycle between the active guanosine triphosphate-bound and inactive guanosine diphosphate-bound forms. RalGTPase-activating protein (RalGAP) complex exerts a negative regulation. Currently, the role of Ral up-regulation in cancers remains unclear.
View Article and Find Full Text PDFBackground & Aims: Mutational profiling of patient tumors has suggested that hepatocellular carcinoma (HCC) development is mainly driven by loss-of-function mutations in tumor suppressor genes. p90 ribosomal S6 kinase 2 (RSK2) functions as a direct downstream kinase of ERK1/2 and elevated RSK2 expression has been reported to support oncogenic functions in some cancers. We investigated if RSK2 was also dysregulated by inactivating mutations in cancers including HCC.
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