Published in Cancer Letters
• Proteins maturation by the proprotein convertases plays important role in inflammation-related cancer and metastasis. • Protein precursors require the proprotein convertases for the induction of inflammation. • Understanding of the molecular mechanism linking the proprotein convertases to inflammation will allow novel therapies. • Inhibitors of t...
The Epidermal Growth Factor Receptor (EGFR) and the Transforming Growth Factor-beta (TGF-beta) are key regulators of hepatocarcinogenesis. Targeting EGFR was proposed as a promising therapy; however, poor success was obtained in human hepatocellular carcinoma (HCC) clinical trials. Here, we describe how EGFR is frequently downregulated in HCC patie...
Published in Cancer Letters
• Shc binds to Erk and sequesters it from MAPK signal transduction. • Inhibition of PTB domain binding to EGFR prevents release of Erk. • In silico screen identified indomethacin, a known NSAID, as an inhibitor for Shc PTB. • Indomethacin indirectly inhibits MAPK signalling by depriving the pathway of Erk. • The approach to MAPK inhibition through ...
Published in Cancer Letters
• Cancer stem cells (CSCs) are the culprits for cancer drug resistance and cancer relapse. • Dietary phytochemicals (curcumin, resveratrol, epigallocatechin gallate) target CSCs. • Repositioned drugs (metformin, niclosamide, thioridazine) target CSCs. • Phytochemical-drug combinations targeting CSCs may exhibit synergistic effects.
Published in Cancer Letters
Polysulfanes show chemopreventive effects against gastrointestinal tumors. We identified diallyl tetrasulfide and its derivative, dibenzyl tetrasulfide (DBTTS), to be mitotic inhibitors and apoptosis inducers. Here, we translate their application in colorectal cancer (CRC). MALDI-TOF-MS analysis identified both compounds as reversible tubulin binde...
Published in Cancer letters
The covalent attachment of β-D-N-acetylglucosamine monosaccharides (O-GlcNAc) to serine/threonine residues of nuclear and cytoplasmic proteins is a major regulatory mechanism in cell physiology. Aberrant O-GlcNAc modification of signaling proteins, metabolic enzymes, and transcriptional and epigenetic regulators has been implicated in cancer. Relen...
Published in Cancer Letters
Recent studies show that metabolic patterns typical of cancer cells, including aerobic glycolysis and increased lipogenesis, are not unique to malignancy, but rather originate in physiologic development. In the postnatal brain, where sufficient oxygen for energy metabolism is scrupulously maintained, neural progenitors nevertheless metabolize gluco...
Published in Cancer letters
Cancer metabolism has been extensively investigated by various tools, and the fact of diverse metabolic reprogramming in cancer cells has been gradually unveiled. In this review, we discuss some contributions in cancer metabolism by general proteomic analysis and post-translational modification analysis using mass spectrometry (MS) technique. Inste...
Published in Cancer Letters
Cancer cells are characterized by sustained proliferative signaling, insensitivity to growth suppressors and resistance to apoptosis as well as by replicative immortality, the capacity to induce angiogenesis and to perform invasive growth. Additional hallmarks of cancer cells include the reprogramming of energy metabolism as well as the ability to ...
Published in Cancer Letters
Cells reprogram their metabolism very early during carcinogenesis; this event is critical for the establishment of other cancer hallmarks. Many oncogenes and tumor suppressor genes control metabolism by interplaying with the existing nutrient-sensing intracellular pathways. Mammalian target of rapamycin, mTOR, is emerging as a collector and sorter ...
