Breast cancer apoptosis

Curcumin is reported to induce breast cancer apoptosis by adaptable the exposure to atmosphere of apoptosis joined genes. Lv et al. applied microarray hybridization of lone-tech apoptotic arrays gone labeled first-strand probes of firm RNA to analyze and describe the genes, which were regulated by curcumin in human breast cancer cells. In MCF-7 cells, genes HIAP1, CRAF1, GADD45, HPRT, MCL-1, BCL2L2, NIP1, TRAP3, GSTP1, PIG11, DAXX, PIG3, RBP2, and JNK1 were upregulated, though genes TRAIL, AP13, TNFR, SARP3, TRAIL-R2, TNFRSF5, TNFb, and hTRIP were downregulated.

Curcumin was as well as reported to reorganize the apoptosisrelated proteins. Exerting the antiapoptotic discharge adherence by blocking lead-apoptotic counterparts, Bcl-2 inhibited the extrinsic apoptosis lane. Induced by curcumin, the antiapoptoticprotein Bcl-2 increased, though the lead-apoptotic protein Bax decreased, leading to an elevated Bax/Bcl-2 ratio. Sun et al. studied the curcumin treatment upon triple-negative breast cancer (TNBC) and found that these cells significantly inhibited the phosphorylation levels of endothelial ensue factor receptor (EGFR) and downstream signaling molecules, such as ERK1/2. Recent studies reported that curcumin enhanced the TNF-fused apoptosis-inducing ligand (TRAIL)induced apoptosis even in TRAIL-resistant breast cancer cells. Moreover, telomerase brawl was inhibited by curcumin through downregulating the aeration of hTERT (telomerase reverse transcriptase).

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