76554-75-1Relevant academic research and scientific papers
Chalcone HTMC causes in vitro selective cytotoxicity, cell-cycle G 1 phase arrest through p53-dependent pathway in human lung adenocarcinoma A549 cells, and in vivo tumor growth suppression
Rao, Yerra Koteswara,Kao, Te-Yu,Ko, Jiunn-Liang,Tzeng, Yew-Min
, p. 6508 - 6512 (2010)
The present Letter identified 2′-hydroxy-2,3,4′,6′- tetramethoxychalcone (HTMC) as a potent in vitro cytotoxic agent with selective activity against cell lines derived from human lung cancer. In A549 lung adenocarcinoma cells, HTMC caused G1 phase cell-cycle arrest. HTMC treatment also led to an inhibition of cell-cycle regulatory proteins phosphorylation of cdc2 (Tyr15 and Tyr161) and Rb (Ser795 and Ser807/811), which was accompanied by the accumulation of tumor suppresser genes p53 and p21. In addition, in vivo data demonstrated that HTMC act as a tumor growth suppressing agent.
Identification of small molecule inhibitors of telomerase activity through transcriptional regulation of hTERT and calcium induction pathway in human lung adenocarcinoma A549 cells
Rao, Yerra Koteswara,Kao, Te-Yu,Wu, Ming-Fang,Ko, Jiunn-Liang,Tzeng, Yew-Min
, p. 6987 - 6994 (2010)
High telomerase activity (TA) is detected in most cancer cells; and thus, TA inhibition by drug or dietary food components is a new strategy for cancer prevention. In this report, we examined the effects of fourteen natural or synthetic compounds on TA in human lung adenocarcinoma A549 cells. The results demonstrated that some of the tested compounds inhibited TA, being 2′-hydroxy-2,3,4′,6′-tetramethoxychalcone (HTMC) was the most potent among tested. In A549 cells, HTMC also inhibited the cell proliferation, decreased the expression of human telomerase reverse transcriptase (hTERT) and sequentially reduced the hTERT promoter. In soft agar assay HTMC treatment reduced the colony formation of A549 cells. Cellular fractionation and immunofluorescence assay demonstrated that there was no translocation of hTERT from nuclei to cytoplasm. Further studies revealed that the release of Ca 2+ was the underlying mechanism of suppressed TA and hTERT transcription in A549 cells exposed to HTMC. These in vitro data support the development of HTMC as a therapeutic agent for cancer complications.
