Inhibition of 12-lipoxygenase during baicalein-induced human lung nonsmall carcinoma H460 cell apoptosis

Leung, Henry W.C.; Yang, Wenhui; Lai, M.-Y.; Lin, Chia‐Der; Lee, H.Z.

doi:10.1016/j.fct.2006.08.021

Cited by 71 publications

(46 citation statements)

References 20 publications

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“…In this report, we showed for the first time that a flavonoid, baicalein, can up-regulate DR5 expression and overcome TRAIL resistance in cancer cells. Baicalein has also been reported to suppress the proliferation of various cancer cells by causing the down-regulation of Bcl-2 expression (3,28). However, in this study, Bcl-2 protein was not changed by baicalein.…”

Section: Discussioncontrasting

confidence: 63%

Baicalein Overcomes Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand Resistance via Two Different Cell-Specific Pathways in Cancer Cells but not in Normal Cells

Taniguchi

Yoshida²,

Horinaka³

et al. 2008

Cancer Research

109

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Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is one of the most promising candidates for new cancer therapeutics. A current problem is that some cancers still remain resistant to TRAIL. We show for the first time that a naturally occurring flavonoid, baicalein, overcomes TRAIL resistance in cancer cells. The combination of baicalein and TRAIL effectively induced apoptosis in TRAIL-resistant colon cancer SW480 cells. Baicalein up-regulated the expression of death receptor 5 (DR5) among TRAIL receptors at the mRNA and protein levels. Suppression of this up-regulation with small interfering RNA (siRNA) efficiently reduced the apoptosis induced by TRAIL and baicalein, suggesting that the sensitization was mediated through DR5 induction. Moreover, baicalein also overcame TRAIL resistance with DR5 upregulation in prostate cancer PC3 cells. Of note, the combination of TRAIL and baicalein hardly induced apoptosis in normal human cells, such as blood cells and hepatocytes. Baicalein increased DR5 promoter activity, and this enhanced activity was diminished by mutation of a CCAAT/enhancerbinding protein homologous protein (CHOP)-binding site in SW480 cells. In SW480 cells, CHOP siRNA blocked both functions of baicalein. CHOP expression was induced by baicalein in SW480 cells; however, in PC3 cells, baicalein scarcely induced CHOP and mutation of the CHOP-binding site did not abrogate the DR5 promoter activation by baicalein. Interestingly, baicalein induced reactive oxygen species (ROS) and a ROS scavenger prevented DR5 expression and TRAIL sensitization in PC3 but not SW480 cells. These results indicate that, using two different pathways, baicalein exposes cancer surveillance of TRAIL and overcomes TRAIL resistance in cancer cells. [Cancer Res 2008;68(21):8918-27]

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Section: Discussioncontrasting

confidence: 63%

Baicalein Overcomes Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand Resistance via Two Different Cell-Specific Pathways in Cancer Cells but not in Normal Cells

Taniguchi

Yoshida²,

Horinaka³

et al. 2008

Cancer Research

109

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“…The major constituents of Scutellaria are baicalin, baicalein and wogonin, the bioactive flavones. These phytochemicals are cytotoxic to various lung cancer cell lines and suppress tumor growth in vivo without systemic toxicity (20,21). The antitumor functions of these flavones are primarily due to their abilities to induce cell cycle arrest, regulate apoptosis-related proteins expression, eliminate adhesion and migration capacities and inhibit metastasis (22,23).…”

Section: Flavonoid Components In Scutellaria Baicalensis Inhibit Nicomentioning

confidence: 99%

Flavonoid components in Scutellaria baicalensis inhibit nicotine-induced proliferation, metastasis and lung cancer-associated inflammation in vitro

Gong

Liu

et al. 2014

International Journal of Oncology

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Abstract. The objective of the present study was to investigate the therapeutic efficacy of flavonoid components in Scutellaria baicalensis on proliferation, metastasis and lung cancer-associated inflammation during nicotine induction in the A549 and H1299 lung cancer cell lines. After experimental period, augmentation of proliferation was observed, accompanied by marked decrease in apoptotic cells in nicotine-induced lung cancer cells; additionally, nicotine-exposed cells exhibited increased invasive and migratory abilities based on invasion and wound-healing assay. Flavones in Scutellaria, baicalin, baicalein and wogonin significantly counteracted the above deleterious changes. Moreover, assessment of tumor apoptotic and metastatic factors on mRNA levels by quantitative PCR and protein levels by western blotting revealed that these phytochemical treatments effectively negated nicotine-induced upregulated expression of bcl-2, bcl-2/bax ratio, caspase-3, matrix metalloproteinase (MMP)-2 and MMP-9 as well as downregulated expression of bax. Further analysis of inflammatory markers such as tumor necrosis factor (TNF)-α and interleukin (IL)-6 in cell culture supernatant and mRNA and protein expression of nuclear transcription factor-kappaB (NF-κB) and I kappa B-alpha (IκB-α) was carried out to substantiate the anti-inflammatory effect of flavones in Scutellaria in nicotine-exposed lung cancer cells. The therapeutic effects observed in the present study are attributed to the potent potential against proliferation, metastasis and inflammatory microenvironment by flavonoid components in Scutellaria in nicotine-induced lung cancer cells.

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“…However, for advanced or metastatic diseases, limited therapeutic options are available (29). Additionally, conventional chemotherapy and radiotherapy often have severe side effects on healthy cells and tissues (30). As a result, the most promising drugs are those with low cytotoxicity, target selectivity and availability for chronic treatment.…”

Section: Discussionmentioning

confidence: 99%

TT‑1, an analog of melittin, triggers apoptosis in human thyroid cancer TT cells via regulating caspase, Bcl‑2 and Bax

Wan

Zhang

et al. 2017

Oncol Lett

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Abstract. Melittin is a 26 amino acid residue antimicrobial peptide with known antitumor activity. In the present study, a novel peptide TT-1, derived from melittin and contained only 11 amino acids, was designed, and its antitumor effect was investigated. The present study is aimed to elucidate the effects and relative mechanisms of TT-1 on a human thyroid cancer cell line (TT) in vitro and in vivo. Cell viability assays, Annexin V/propidium iodide assays, western blotting and quantitative reverse transcription polymerase chain reaction were performed. Furthermore, a tumor-xenograft model was established to investigate the apoptotic mechanisms of TT-1 on TT cells. The results obtained indicated that TT-1 was able to suppress the proliferation of TT cells and exhibited low cytotoxicity to normal thyroid cells in vitro. The apoptotic rates of TT cells were also increased following TT-1 treatment. Additionally, TT-1 stimulated caspase-3, caspase-9 and Bax, and inhibited B-cell lymphoma 2 mRNA and protein expression. Finally, it was also demonstrated that TT-1 is able to markedly suppress tumor growth in a TT-bearing nude mouse model. In summary, TT-1 may inhibit the proliferation of TT cells by inducing apoptosis in vitro and in vivo, indicating that TT-1 may be a potential candidate for the treatment of thyroid cancer.

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Inhibition of 12-lipoxygenase during baicalein-induced human lung nonsmall carcinoma H460 cell apoptosis

Cited by 71 publications

References 20 publications

Baicalein Overcomes Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand Resistance via Two Different Cell-Specific Pathways in Cancer Cells but not in Normal Cells

Baicalein Overcomes Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand Resistance via Two Different Cell-Specific Pathways in Cancer Cells but not in Normal Cells

Flavonoid components in Scutellaria baicalensis inhibit nicotine-induced proliferation, metastasis and lung cancer-associated inflammation in vitro

TT‑1, an analog of melittin, triggers apoptosis in human thyroid cancer TT cells via regulating caspase, Bcl‑2 and Bax

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