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(C and D) Characteristic absorption peaks of (AĪnd B) Design and skeleton of structurally stable double carbonylĪnalogs of curcumin. Stability and antitumor activity than curcumin.Ĭharacteristic absorption peaks of compound A17 and curcumin. 1), and described its stability andĪntitumor activity. In the present study, we identified a novel doubleĬarbonyl analog of curcumin (named A17 Fig. Respectively 06, andĪnalogs of curcumin which can enhance stability and anticancerĮffects, we designed and screened novel double carbonyl analogs ofĬurcumin. Them were discovered as the most efficient compounds against tumorĬells with enhanced stability. We designed many mono-carbonyl analogs of curcumin and three of Instability and poor metabolic properties, by deleting this moiety, Given that the β-diketone moiety of curcumin may lead to its Laboratory, in order to enhance its metabolic stability and

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Years, a series of curcumin analogs have been synthesized in our Of cucurmin have significantly limited its clinical application However, the instability and poor metabolic property Non-small cell lung cancer H460 cells ( 13) and human liposarcoma cells ( 14). Its pro-apoptotic effects by inducing ER stress in acute Native chemoprevention agent in pancreatic and colon cancerĬurcumin may induce the apoptosis of several types of cancer cells A few clinical trials have demonstrated thatĬurcumin possesses anticancer effect, but was proposed as a more Various bio-functions of curcumin have been revealed throughĮxtensive research. Curcumin, a yellow compound, is isolated from the rhizome Various anticancer agents, such as paclitaxel ( 4), farnesol ( 5) and polyphyllin D ( 6), can induce cancer cell apoptosis by ER Have attracted much attention for anticancer therapy ( 2, 3). That effectively enhance tumor cell death by activating ER stress

Pathophysiology of cancer therefore pharmacological interventions Yet, prolonged ER stress canĪctivate apoptotic pathways of damaged cells ( 1). Previous studies have shown that the perturbation ofĮndoplasmic reticulum (ER) function causes ER stress, which hasīeen linked to numerous diseases. These results imply that A17 could be further explored as a potential anticancer agent for the treatment of human non-small cell lung cancer (NSCLC). Our studies demonstrated that A17 has better stability and antitumor activity than curcumin in H460 cells via an ER stress-mediated mechanism. When CHOP was knocked down by specific siRNA, A17-induced cell apoptosis was attenuated, thereby further demonstrating that the apoptotic pathway is ER stress‑dependent. The results showed that A17 not only induced CHOP expression in human lung cancer H460 cells, but also induced the apoptosis of H460 cells in a dose-responsive manner, and this effect was related to corresponding activation of some important components in the endoplasmic reticulum (ER) stress-mediated apoptosis pathway. In the present study, we screened a double carbonyl analog of curcumin (A17) and analyzed its effects and mechanism of inducing apoptosis in human lung cancer H460 cells. See identical proteins and their annotated locations for NP_012861.Curcumin can inhibit the growth of a variety of cancer cells however, its poor bioavailability and pharmacokinetic profiles, which are attributed to its instability under physiological conditions, have limited its application in anticancer therapy.

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NM_001179628.1 → NP_012861.1 TPA: stress-responsive transcriptional activator MSN4

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NC_001143.9 Reference assembly Range 323228.325120 Download GenBank, FASTA, Sequence Viewer (Graphics)

Model RNAs and proteins are also reported here. RefSeqs for chromosomes and scaffolds (contigs) from both reference and alternateĪssemblies. Sequences (RefSeqs) from all assemblies on which this gene is annotated, such as The following sections contain reference sequences that belong to a

Stress finder activator