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Curcumin Induces Cell Death and Restores Tamoxifen Sensitivity in the Antiestrogen-Resistant Breast Cancer Cell Lines MCF-7/LCC2 and MCF-7/LCC9
Investigation of the efficacy of curcumin alone and in combination with tamoxifen in the established antiestrogen-resistant breast cancer cell lines MCF-7/LCC2 and MCf-7-LCC9 suggested that curcumins alone and combinations ofCurcumin with endocrine therapy may be of therapeutic benefit for endocrine- resistant breast cancer.
A novel long non-coding RNA-ARA: adriamycin resistance-associated.
Marine-derived chromopeptide A, a novel class I HDAC inhibitor, suppresses human prostate cancer cell proliferation and migration
The results identify chromopeptide A as a novel class I HDAC inhibitor and provide therapeutic strategies that may be implemented in prostate cancer.
α2,6-hyposialylation of c-Met abolishes cell motility of ST6Gal-I-knockdown HCT116 cells
The hyposialylation of c-Met can abolish cell motility in ST6Gal-I-KD HCT116 cells, and this selectively altered cell migration was caused by the loss of α2,6-sialic acid structures on c- met.
Aspirin Inhibits Cancer Metastasis and Angiogenesis via Targeting Heparanase
Insightful insights are provided for a better understanding of the mechanisms of aspirin in anticancer effects, and a direction for the development of small-molecule inhibitors of heparanase is offered.
O-GlcNAcylation of Cofilin Promotes Breast Cancer Cell Invasion*
This study determined that the actin-binding protein cofilin is O-GlcNAcylated by OGT and mainly, if not completely, mediates OGT modulation of cell mobility.
c-Myc alterations confer therapeutic response and acquired resistance to c-Met inhibitors in MET-addicted cancers.
It is reported that the transcriptional factor c-Myc functions as a downstream effector to dictate the therapeutic response to c-Met inhibitors in c- Met-addicted cancer and derived resistance, offering a preclinical proof of concept for the application of c- myc-blocking agents as a tactic to thwart resistance to kinase inhibitors.
FS-93, an Hsp90 inhibitor, induces G2/M arrest and apoptosis via the degradation of client proteins in oncogene addicted and derived resistant cancer cells
It is described that FS-93, a potent Hsp90 inhibitor, impacted the survival of several types of oncogene addicted cancer cells through inducing G2/M arrest and apoptosis and implicates that targeting HSp90 is a promising alternative therapeutic tactic in oncogen addicted and derived resistant cancer cells.