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Dual action on promoter demethylation and chromatin by an isothiocyanate restored GSTP1 silenced in prostate cancer
- L. Wang, A. Beklemisheva, X. Liu, A. Ferrari, J. Feng, J. Chiao
- Biology, Medicine
- Molecular carcinogenesis
- 1 January 2007
The PEITC‐mediated cross‐talk between the DNA and chromatin in demethylating and reactivating GSTP1 genes, which is critically inactivated in prostate carcinogenesis, underlines a primary mechanism of cancer chemoprevention. Expand
De-repression of the p21 promoter in prostate cancer cells by an isothiocyanate via inhibition of HDACs and c-Myc.
The PEITC-mediated growth attenuation of prostate cancer cells includes an interactive mechanism involving HDAC and c-Myc inhibition, suggesting that the inhibition of HDACs may be the primary mechanism for p21 activation. Expand
Overexpressed androgen receptor linked to p21WAF1 silencing may be responsible for androgen independence and resistance to apoptosis of a prostate cancer cell line.
The functional link between AR dosage and p21WAF1 expression suggests that therapeutic reduction of AR protein in advanced prostate cancers with elevated AR levels may re-establish their hormone dependence and improve therapeutic response to repeated hormonal ablation and/or induction of apoptosis. Expand
Down-regulation of prostate-specific antigen expression by finasteride through inhibition of complex formation between androgen receptor and steroid receptor-binding consensus in the promoter of the…
The data indicate that inhibition of complex formation between SRBC and nuclear proteins due to the remarkable decrease in the level of androgen receptor plays a key role in the down-regulation of PSA gene expression by finasteride in LNCaP cells. Expand
Phosphorylation/dephosphorylation of androgen receptor as a determinant of androgen agonistic or antagonistic activity.
- L. Wang, X. Liu, W. Kreis, D. Budman
- Biology, Medicine
- Biochemical and biophysical research…
- 27 May 1999
It is demonstrated that androgen receptor phosphorylation determines whether or not AR ligands perform as agonists or antagonists in LNCaP cells, and that the phosphorylated androgen receptors is the form of the receptor transcriptionally active in regulation. Expand
Androgen antagonistic effect of estramustine phosphate (EMP) metabolites on wild-type and mutated androgen receptor.
The data indicate that estramustine phosphate metabolites perform as androgen antagonists of AR, an additional mechanism involved in the therapeutic effect of estramUSTine phosphate in patients with prostate cancer. Expand
Repression of androgen receptor in prostate cancer cells by phenethyl isothiocyanate.
With the AR modulation and growth attenuation, PEITC and possibly other isothiocyanates, may prevent and inhibit hormone sensitive and refractory prostate cancer. Expand
Differential effect of vinorelbine versus paclitaxel on ERK2 kinase activity during apoptosis in MCF-7 cells
- X. Liu, L. Wang, W. Kreis, D. Budman, L. Adams
- Biology, Medicine
- British Journal of Cancer
- 1 September 2001
The data suggest that the apoptosis induced by vinorelbine in MCF-7 cells is mediated through the bcl-2 phosphorylation/bax/caspases pathways, and that activation of ERK2 by vInorlbine does not directly lead to the drug-mediated apoptosis. Expand
Pharmacological studies of meisoindigo: absorption and mechanism of action.
- X. Ji, X. Liu, K. Li, R. H. Chen, L. Wang
- Chemistry, Medicine
- Biomedical and environmental sciences : BES
- 1 September 1991
Experiments have shown the improved absorption of meisoindigo, compared to indirubin to be one of the major reasons for the enhancement of antitumor activity. Expand
Synergism of Cytotoxic Effects of Vinorelbine and Paclitaxel in Vitro
These studies suggest concurrent administration of these two agents may lead to a less than optimal cytotoxic result and Sequential exposure of vinorelbine preceding paclitaxel or prolonged exposure to both agents concurrently needs to be tested clinically to determine whether the antitumor activity of this combination can be enhanced. Expand