scholarly journals Identification of Candidate Genes Determining Chemosensitivity to Anti-cancer Drugs of Gastric Cancer Cell Lines

2009 ◽  
Vol 32 (11) ◽  
pp. 1936-1939 ◽  
Author(s):  
Tomoki Nakamura ◽  
Noriyuki Nakatsu ◽  
Yoko Yoshida ◽  
Kanami Yamazaki ◽  
Shingo Dan ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Candidate Genes ◽  
Cell Lines ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Cancer Cell Lines ◽  
Cancer Drugs ◽  
Anti Cancer ◽  
Gastric Cancer Cell Lines

The activity of CKD601, telomerase inhibitor, against gastric cancer cell lines and resistance mechanism, which is associated with hTERT expression and ALT

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 13126-13126
Author(s):  
J. Jung ◽  
Y. Park ◽  
H. Jong ◽  
S. Im ◽  
Y. Song ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Resistance Mechanism ◽  
Cancer Cell Lines ◽  
Telomerase Activity ◽  
Telomerase Inhibitor ◽  
Anti Cancer ◽  
Gastric Cancer Cell Lines

13126 Background: CKD601, a newly developed telomerase inhibitor, shows an anti-cancer effect through its inhibitory effect on telomerase, by intercalation of the drug into the structures of the G-quadruplex. No study has been conducted to assess the anti-cancer effects of CKD601 in regards to gastric cancer. We attempted to confirm the anti-cancer effect of CKD601 in the gastric cancer cell line, and to investigate the mechanisms of the anti-cancer effect and resistance in some cell lines. Methods: After long-term drug exposure, we performed Southern analysis, TRAP, and β-Gal staining about the extracted DNA, RNA, and protein from the gastric cancer cell lines and the U2OS cell line to confirm the anti-cancer effect of CKD601. We attempted to investigate the change in the hTERT expression of cancer cells as a result of exposure to CKD601 by RT-PCR and real-time PCR, and to confirm the presence of the ALT (alternate lengthening of telomere) mechanism by metaphase telomere FISH and IF. Results: The anticancer effect of CKD601, including the shortening of telomere, inhibition of telomerase activity, cellular aging, and decreased growth rates, was observed in some gastric cancer cell lines (SNU-1 and SNU-601). SNU-484 and SNU-668 cell lines showed no anti-cancer effect of CKD601. The resistance mechanism of SNU-484 was the significant overexpression of hTERT following exposure to CKD601. ALT, another mechanism that functions in the maintenance of telomere length, was detected in SNU-668 following exposure to CKD601, and it is the resistance mechanism against CKD601. Conclusions: CKD601 is active in gastric cancer by the inhibition of telomerase activity. The resistance mechanisms of gastric cancer cell lines against CKD601 are the induction of the overexpression of hTERT and the ALT mechanism. [Table: see text] No significant financial relationships to disclose.

Let-7a Could Serve as A Biomarker for Chemo-Responsiveness to Docetaxel in Gastric Cancer

2019 ◽  
Vol 19 (3) ◽  
pp. 304-309 ◽  
Author(s):  
Najibeh Shekari ◽  
Faezeh Asghari ◽  
Navideh Haghnavaz ◽  
Dariush Shanehbandi ◽  
Vahid Khaze ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Mtt Assay ◽  
Gastric Cancer Cell ◽  
Target Genes ◽  
Cancer Cell Lines ◽  
Expression Level ◽  
Anti Cancer ◽  
Gastric Cancer Cell Lines

Background: MicroRNAs are noncoding RNAs which play critical roles in response to anti-cancer agents. Let-7a and miR-21 are well-known tumor-suppressor and oncomiR miRNAs, respectively. They are involved in tumorigenesis of gastric cancer and have potential to be used as markers in response to the therapy. Objective: We aimed to study alterations in the expression of Let-7a and miR-21, and their targets in gastric cancer cell lines after treatment with docetaxel. Methods: In order to determine the IC50 of docetaxel, MTT assay was performed in AGS, MKN45 and KATO III gastric cancer cell lines. The expression levels of Let-7a and miR-21 and their target genes, HMGA2 and PDCD4, were determined by reverse-transcription quantitative real-time PCR for both treated and untreated cell lines. Results: MTT assay showed higher IC50 concentration of docetaxel in KATO III in comparison with AGS and MKN45, indicating KATO III`s higher resistance to docetaxel. Following the treatment, the expression level of Let-7a was significantly increased in AGS and MKN45, while decreased in KATO III. Expression level of miR- 21 in the three treated cell lines was increased significantly. Not only Let-7a, but also expression level of HMGA2 and PDCD4 genes showed different patterns in KATO III in comparison with AGS and MKN45. Conclusion: Down-regulation and up-regulation of Let-7a in docetaxel-resistant and sensitive cell lines, respectively indicates its potential usefulness as biomarker for responsiveness of gastric cancer to the therapy with docetaxel and also for predicting patient`s outcome.

Pharmacological Synergism Between Cannabinoids and Paclitaxel in Gastric Cancer Cell Lines

2009 ◽  
Vol 155 (1) ◽  
pp. 40-47 ◽  
Author(s):  
Hideyo Miyato ◽  
Joji Kitayama ◽  
Hiroharu Yamashita ◽  
Daisuke Souma ◽  
Masahiro Asakage ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Cancer Cell Lines ◽  
Gastric Cancer Cell Lines

Low-Dose Oxaliplatin Enhances the Antitumor Efficacy of Paclitaxel in Human Gastric Cancer Cell Lines

Digestion ◽  
2006 ◽  
Vol 74 (1) ◽  
pp. 19-27 ◽  
Author(s):  
Jinyu Gu ◽  
Hirofumi Yamamoto ◽  
Xueying Lu ◽  
Chew Yee Ngan ◽  
Tadashi Tsujino ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Low Dose ◽  
Cancer Cell Lines ◽  
Antitumor Efficacy ◽  
Human Gastric Cancer ◽  
Human Gastric Cancer Cell ◽  
Gastric Cancer Cell Lines

scholarly journals Inhibition of cell proliferation in gastric cancer cell lines on exposure to rubriflordilactone A

2015 ◽  
Vol 11 (1) ◽  
pp. 63
Author(s):  
Shang-Jin Peng ◽  
Jue-Wei Chen
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Underlying Mechanism ◽  
Cancer Cell Lines ◽  
Epithelial Cell Line ◽  
Similar Reduction ◽  
Gastric Cancer Cell Lines

<p class="Abstract">The present study investigates the effect of rubriflordilactone A on the viability and its underlying mechanism in gastric cancer cell lines (SNU-1 and SNU-5) and normal gastric epithelial cell line (GES‑1). Incubation of the gastric cancer and non cancer cell lines in acidic media led to reduction in the viability of the non cancer cells without any effect on cancer cells. Apoptosis in SNU-1 and SNU-5 cells was induced on exposure to rubriflordilactone A after 48 hours compared to the control cells (p&lt;0.01). The percentage of apoptosis in SNU-1 and SNU-5 cells on exposure to rubriflordilactone A was 79.3 ± 4.7 and 74.0 ± 5.1, respectively after 48 hours. Exposure of SNU-1 and SNU-5 cancer cell lines to rubriflordilactone A at a concentration of 10 μM in media with acidic pH decreased phosphorylation of ERK ½. The similar reduction was caused by ERK 1/2 phosphorylation inhibition, PD98059. Thus rubriflordilactone A reduces viability of gastric cancer cell lines by inducing apoptosis through the reduction of ERK 1/2 phosphorylation.</p><p> </p>

High-density allelotype of the commonly studied gastric cancer cell lines

2001 ◽  
Vol 32 (1) ◽  
pp. 67-81 ◽  
Author(s):  
Yun-Ling Zheng ◽  
Alison M. Herr ◽  
Blake A. Jacobson ◽  
Lance J. Ferrin
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Cancer Cell Lines ◽  
High Density ◽  
Gastric Cancer Cell Lines
Sign in / Sign up

Export Citation Format

Share Document