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Bin Chuan Ji

Researcher at Chienkuo Technology University

Publications -  12
Citations -  278

Bin Chuan Ji is an academic researcher from Chienkuo Technology University. The author has contributed to research in topics: Apoptosis & Cancer cell. The author has an hindex of 10, co-authored 12 publications receiving 246 citations.

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Journal Article

Phenethyl Isothiocyanate (PEITC) Promotes G2/M Phase Arrest via p53 Expression and Induces Apoptosis through Caspase- and Mitochondria-dependent Signaling Pathways in Human Prostate Cancer DU 145 Cells

TL;DR: It is found that PEITC induced a dose-dependent decrease in cell viability through induction of cell apoptosis and cell cycle arrest in the G(2)/M phase of DU 145 cells and might exhibit anticancer activity and become a potent agent for human prostate cancer cells in the future.
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Triptolide induced DNA damage in A375.S2 human malignant melanoma cells is mediated via reduction of DNA repair genes

TL;DR: Observations indicated that triptolide induced DNA damage and inhibitedDNA damage and repair-associated gene expression (mRNA) that may be factors for triptoide-mediated inhibition of cell growth in vitro in A375.S2 cells.
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Gallic acid provokes DNA damage and suppresses DNA repair gene expression in human prostate cancer PC-3 cells

TL;DR: It is shown that gallic acid caused DNA damage and inhibited DNA repair genes as well as both effects may be the critical factors for GA‐inhibited growth of PC‐3 cells in vitro.
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Bisdemethoxycurcumin-induced S phase arrest through the inhibition of cyclin A and E and induction of apoptosis via endoplasmic reticulum stress and mitochondria-dependent pathways in human lung cancer NCI H460 cells

TL;DR: Investigation of the effect of BDMC on the cell death via the cell cycle arrest and induction of apoptosis in NCI H460 human lung cancer cells suggests that BDMC induced cell apoptosis through multiple signal pathways such as extrinsic, intrinsic and ES tress pathway.
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Demethoxycurcumin induces the apoptosis of human lung cancer NCI-H460 cells through the mitochondrial-dependent pathway.

TL;DR: DMC significantly induced cell morphological changes and decreased the percentage of viable NCI-H460 cells and DMC induced apoptosis based on the cell distribution in the sub-G1 phase and it is suggested that DMC may be used as a novel anticancer agent for the treatment of lung cancer in the future.