• Journal of Life Science
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• v.17 no.9 s.89
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• pp.1232-1236
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• 2007

Growth and DNA synthesis inhibitory effects of extracts from root bark of Ulmus parvifolia on MG-63 human osteosarcoma cells, HT-29 human colon cancer cells and K-562 leukemia cancer cells were studied. The root bark extract of Ulmus parvifolia was extracted with methanol, hot water and juice. The methanol extract showed the highest inhibitory effect on growth of MG-63, HT-29 and K-562 cancer cells by >85%. The treatment of hot water and juice extracts from root bark of Ulmus parvifolia also inhibited growth of the above cancer cells with increasing concentration. DNA synthesis of MG-63 and HT-29 cancer cells was significantly inhibited by adding methanol, hot water and juice extracts from root bark of Ulmus parvifolia with increasing concentration, showing that the inhibitory effect of growth was more effective on HT-29 cancer cells. These results suggest that the methanol extract from root bark of Ulmus parvifolia may have specific active com-pounds on anticancer effect. The hot water extract also showed a strong inhibitory effect on growth of cancer cells, indicating that the active compounds may be stable to heat.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.8
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• pp.3653-3656
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• 2012

Background: A number of effective prevention measures have been introduced in attempts to substantially reduce both the incidence and mortality due to many kinds of cancer. The search for new anti-cancer compounds in foods or in plant medicines is one realistic and promising approach to prevention. Chinese medicines provide a rich pool of novel and efficacious agents for cancer prevention and treatment. Previously it was demonstratrated that hyperin extracted from the Manchurian rhododendron leaf reduces the proliferation of many cancer cells. The present study was carried out to evaluate its effects on human endometrial cancer cell viability and apoptosis and to investigate its mechanisms of action in RL952 cells. Methods: Cell viability was measured using the MTT assay. Intracellular calcium ions were detected using laser-scanning confocal microscopy. The effects of hyperin on apoptosis related proteins in RL952 cells were examined using Western blot analysis. Results: The growth of RL952 cells was inhibited by treatment with hyperin. OD values of caspase-3 and caspase-9 were increased and expression of bcl-2 was increased and bax was decreased in protein levels in RL952 cells after 24 h of hyperin treatment, Moreover, intracellular calcium accumulation occurred in hyperin-treated cells. Conclusion: These results suggest that hyperin may play an important role in tumor growth suppression by inducing apoptosis in human endometrial cells via a $Ca^{2+}$-related mitochondrion apoptotic pathway in RL952 cells.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.20
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• pp.8631-8635
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• 2014

Glutathione S-transferase A1 (GSTA1) appears to be primarily involved in detoxification processes, but possible roles in lung cancer remain unclear. The objective of this study was to investigate the expression and function of GSTA1 in lung cancer cells. Real-time PCR and Western blotting were performed to assess expression in cancer cell lines and the normal lung cells, then verify the A549 cells line with stable overexpression. Localization of GSTA1 proteins was assessed by cytoimmunofluorescence. Three double-strand DNA oligoRNAs (SiRNAs) were synthesized prior to being transfected into A549 cells with Lipofectamine 2000, and then the most efficient SiRNA was selected. Expression of the GSTA1 gene in the transfected cells was determined by real-time PCR and Western blotting. The viability of the transfected cells were assessed by MTT. Results showed that the mRNA and protein expression of A549 cancer cells was higher than in MRC-5 normal cells. Cytoimmunofluorescence demonstrated GSTA1 localization in the cell cytoplasm and/or membranes. Transfection into A549 cells demonstrated that down-regulated expression could inhibit cell viability. Our data indicated that GSTA1 expression may be a target molecule in early diagnosis and treatment of lung cancer.

• BMB Reports
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• v.53 no.12
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• pp.622-627
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• 2020

Cancer stem cells (CSCs) or tumor-initiating cells are thought to play critical roles in tumorigenesis, metastasis, drug resistance, and tumor recurrence. For the diagnosis and targeted therapy of CSCs, the molecular identity of biomarkers or therapeutic targets for CSCs needs to be clarified. In this study, we identified CD166 as a novel marker expressed in the sphere-forming CSC population of A2780 epithelial ovarian cancer cells and primary ovarian cancer cells. The CD166+ cells isolated from A2780 cells and primary ovarian cancer cells highly expressed CSC markers, including ALDH1a1, OCT4, and SOX2, and ABC transporters, which are implicated in the drug resistance of CSCs. The CD166+ cells exhibited enhanced CSC-like properties, such as increased sphere-forming ability, cell migration and adhesion abilities, resistance to conventional anticancer drugs, and high tumorigenic potential in a xenograft mouse model. Knockdown of CD166 expression in the sphere-forming ovarian CSCs abrogated their CSC-like properties. Moreover, silencing of CD166 expression in the sphere-forming CSCs suppressed the phosphorylation of focal adhesion kinase, paxillin, and SRC. These results suggest that CD166 plays a key role in the regulation of CSC-like properties and focal adhesion kinase signaling in ovarian cancer.

• Herbal Formula Science
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• v.24 no.4
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• pp.283-288
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• 2016

Objectives : The purpose of this study was to investigate the anti-cancer effects of extract of Rhus verniciflua Stokes (RVS) in human breast cancer cell lines. Methods : In cultured human breast cancer MCF-7 cells, we investigated growth inhibitory effect of RVS. MCF-7 cells were cultured with various concentrations (0, 200, 300, and 400 ug/ml) of RVS at $37^{\circ}C$ for 24 h. We performed CCK-8 assay and flow cytometry for detection of Annexin V-PI staining. Results : As a result, RVS inhibits the cell growth and induction of apoptosis in dose dependent manner in MCF-7 breast cancer cells. Conclusion : RVS has anti-cancer activities and induced apoptosis in human breast cancer MCF-7 cells. Therefore we suggest that RVS can use as a novel class of anti-cancer drugs.

• Korean Journal of Pharmacognosy
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• v.42 no.3
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• pp.282-287
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• 2011

This study was presented to the anti-cancer activity from different fraction of Zanthoxylum schnifolium fruits. The values for human colon cancer cell(HT-29) survival rate of 0.3 mg/mL of 70% EtOH and 70% MeOH ethyl acetate fraction extracts were 7.62${\pm}$0.173%, 7.66${\pm}$0.037%, respectively. It was shown that human colon cancer cell(HT-29) survival rate was in a dose-dependent manner. The percentages of cells were increased in the sub-G0 and G0/G1 phase region, meaning that cell proliferation was decreased. The RT-PCR demonstrated that 70% EtOH and 70% MeOH ethyl acetate fraction extracts were down-regulated the expression of Bcl-2 and survivin genes in HT-29 cells. We examined that 70% EtOH and 70% MeOH ethyl acetate fraction extracts anti-cancer activities initiated through ROS generation suggesting that HT-29 cells treated with ethyl acetate fraction extracts induced ROS generation. Our results revealed that the Zanthoxylum schnifolium fruit may expect for anti-cancer activities in HT-29 cells.

• International Journal of Stem Cells
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• v.17 no.3
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• pp.270-283
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• 2024

Glutathione (GSH), the main cellular antioxidant, dynamically influences tumor growth, metastasis, and resistance to therapy in the tumor microenvironment (TME), which comprises cancer cells, immune cells, stromal cells, and non-cellular components, including the extracellular matrix, metabolites, hypoxia, and acidity. Cancer stem cells (CSCs) and T cells are minor but significant cell subsets of the TME. GSH dynamics influences the fate of CSCs and T cells. Here, we explored GSH dynamics in CSCs and T cells within the TME, as well as therapeutic approaches that could target these dynamics.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.4
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• pp.1655-1659
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• 2016

Celecoxib, a selective inhibitor of COX-2, showed cytotoxic effects in many cancer cell lines including cervical cancer cells. This study investigated the effect of celecoxib on cell cycle arrest in HeLa cervical cancer cells through p53 expression. In vitro anticancer activity was determined with the 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) method. A double staining method was applied to investigate the mechanism of cell death, cell cycling was analyzed by flow cytometryand immunocytochemistry was employed to stain p53 expression in cells. Celecoxib showed strong cytotoxic effects and induced apoptosis with an $IC_{50}$ value of $40{\mu}M$. It induced cell cycle arrest at G2/M phase by increasing level of p53 expression on HeLa cells.

• Molecules and Cells
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• v.44 no.8
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• pp.569-579
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• 2021

Cyclase-associated protein 2 (CAP2) has been addressed as a candidate biomarker in various cancer types. Previously, we have shown that CAP2 is expressed during multi-step hepatocarcinogenesis; however, its underlying mechanisms in liver cancer cells are not fully elucidated yet. Here, we demonstrated that endoplasmic reticulum (ER) stress induced CAP2 expression, and which promoted migration and invasion of liver cancer cells. We also found that the ER stress-induced CAP2 expression is mediated through activation of protein kinase C epsilon (PKCε) and the promotor binding of activating transcription factor 2 (ATF2). In addition, we further demonstrated that CAP2 expression promoted epithelial-mesenchymal transition (EMT) through activation of Rac1 and ERK. In conclusion, we suggest that ER stress induces CAP2 expression promoting EMT in liver cancer cells. Our results shed light on the novel functions of CAP2 in the metastatic process of liver cancer cells.

• Yonsei Medical Journal
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• v.59 no.9
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• pp.1041-1048
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• 2018

Purpose: Heat shock factor 1 (HSF1) is a key regulator of the heat shock response and plays an important role in various cancers. However, the role of HSF1 in gastric cancer is still unknown. The present study evaluated the function of HSF1 and related mechanisms in gastric cancer. Materials and Methods: The expression levels of HSF1 in normal and gastric cancer tissues were compared using cDNA microarray data from the NCBI Gene Expression Omnibus (GEO) dataset. The proliferation of gastric cancer cells was analyzed using the WST assay. Transwell migration and invasion assays were used to evaluate the migration and invasion abilities of gastric cancer cells. Protein levels of HSF1 were analyzed using immunohistochemical staining of tissue microarrays from patients with gastric cancer. Results: HSF1 expression was significantly higher in gastric cancer tissue than in normal tissue. Knockdown of HSF1 reduced the proliferation, migration, and invasion of gastric cancer cells, while HSF1 overexpression promoted proliferation, migration, and invasion of gastric cancer cells. Furthermore, HSF1 promoted the proliferation of gastric cancer cells in vivo. In Kaplan-Meier analysis, high levels of HSF1 were associated with poor prognosis for patients with gastric cancer (p=0.028). Conclusion: HSF1 may be closely associated with the proliferation and motility of gastric cancer cells and poor prognosis of patients with gastric cancer. Accordingly, HSF1 could serve as a prognostic marker for gastric cancer.