Publications by authors named "Ji-Na Pak"
To elucidate the underlying antitumor mechanism of lambertianic acid (LA) derived from Pinus koraiensis, the role of cancer metabolism related molecules was investigated in the apoptotic effect of LA in DU145 and PC3 prostate cancer cells. MTT assay for cytotoxicity, RNA interference, cell cycle analysis for sub G1 population, nuclear and cytoplasmic extraction, lactate, Glucose and ATP assay by ELISA, Measurement of reactive oxygen species (ROS) generation, Western blotting, and immunoprecipitation assay were conducted in DU145 and PC3 prostate cancer cells. Herein LA exerted cytotoxicity, increased sub G1 population and attenuated the expression of pro-Caspase3 and pro-poly (ADP-ribose) polymerase (pro-PARP) in DU145 and PC3 cells.
View Article and Find Full Text PDFThe goal of the current study is to assess the antitumor mechanism by the combination (7:3) of Angelica gigas and Torilis japonica (AT) that was found most effective through screening against prostate-specific antigen (PSA) in LNCaP prostate cancer cells. Here, AT reduced the viability and the number of colonies in androgen-dependent LNCaP cells more than in androgen independent PC3 and DU145 cells. Also, AT induced G1 phase arrest, cleaved PARP and caspase 3, activated p27 and decreased the expression of Cyclin D1, Cyclin E, cdk2 in LNCaP cells.
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- The study investigated how melatonin, found in certain edible plants, affects metastasis in colorectal cancer through its interaction with TMPRSS4 and EMT signaling in HCT15 and SW620 cancer cells.
- Melatonin showed limited cytotoxic effects but significantly reduced cancer cell invasiveness and migration, while altering the expression of various proteins related to metastasis.
- The results indicate that melatonin may inhibit metastasis in colon cancer by suppressing TMPRSS4-related processes, enhancing E-cadherin expression, and altering other key signaling pathways.
Article Synopsis
- - The study investigates the apoptotic mechanism of ginsenoside metabolite compound K in colorectal cancer cells, highlighting its superior ability to reduce cell viability and alter key protein expressions compared to control HCT116 cells.
- - Through its effects, compound K was shown to increase sub G1 cell population and decrease levels of proteins associated with survival and proliferation, including LGR5, c-Myc, and procaspase3.
- - Additionally, compound K enhances the effectiveness of traditional chemotherapy drugs like 5-fluorouracil and Doxorubicin, suggesting its potential for combined therapy in treating colorectal cancer by inhibiting LGR5 through a caspase and p53 dependent mechanism.
Here the molecular mechanisms of Kaempferol were examined in colorectal cancers (CRCs). Kaempferol significantly exerted antiproliferative and cytotoxic effect in HCT116, HCT15, and SW480 cells. Also, Kaempferol increased sub G1 population, G2/M arrest, and the numbers of TUNEL cells in HCT116 colorectal cancer cells.
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