scholarly journals microRNA-32 inhibits the proliferation and invasion of the SGC-7901 gastric cancer cell line in vitro

2013 ◽  
Vol 7 (1) ◽  
pp. 270-274 ◽  
Author(s):  
JIANFENG ZHANG ◽  
XIAOLING KUAI ◽  
MENGJIAO SONG ◽  
XIAOQI CHEN ◽  
ZHIHUA YU ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Line ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Gastric Cancer Cell Line ◽  
Cancer Cell Line ◽  
Proliferation And Invasion

scholarly journals Cytosolic Cl- Affects the Anticancer Activity of Paclitaxel in the Gastric Cancer Cell Line, MKN28 Cell

2017 ◽  
Vol 42 (1) ◽  
pp. 68-80 ◽  
Author(s):  
Sachie Tanaka ◽  
Hiroaki Miyazaki ◽  
Atsushi Shiozaki ◽  
Daisuke Ichikawa ◽  
Eigo Otsuji ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cell Line ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Gastric Cancer Cell Line ◽  
Cancer Cell Line ◽  
Tubulin Polymerization ◽  
Pass Through

Background/Aims: Our previous study revealed that cytosolic Cl- affected neurite elongation promoted via assembly of microtubule in rat pheochromocytoma PC12D cells and Cl-–induced blockade of intrinsic GTPase enhanced tubulin polymerization in vitro. Paclitaxel (PTX) is a microtubule-targeted chemotherapeutic drug and stabilizes microtubules resulting in mainly blockade of mitosis at the metaphase-anaphase transition and induction of apoptosis. In the present study, we tried to clarify whether the cytosolic Cl- affected PTX ability to inhibit cell growth in the gastric cancer cell line, MKN28. Methods: To clarify the cytosolic Cl- action on PTX-induced cell death and metaphase-anaphase transition in the gastric cancer cell line, MKN28 cell, and PTX-induced tubulin polymerization, we performed cell proliferation assay, cytosolic Cl- concentration measurement, immunofluorescence microscopy, and in vitro tubulin polymerization assay. Results: The decline of cytosolic Cl- weakened the cytotoxic effect of PTX on cell proliferation of MKN28 cells, which could pass through the metaphase-anaphase transition. Moreover, in vitro PTX-induced tubulin polymerization was diminished under the low Cl- condition. Conclusions: Our results strongly suggest that the upregulation of cytosolic Cl- concentration would enhance the antitumor effect of PTX, and that the cytosolic Cl- would be one of the key targets for anti-cancer therapy.

Effects of Onosma dichroanthum Boiss. root extract on AGS human gastric cancer cell-line

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Mohammad Mostakhdem Hashemi ◽  
Majid Marjani ◽  
Nahid Poursharifi ◽  
Abdoljalal Marjani
Keyword(s):  
Gastric Cancer ◽  
Cell Line ◽  
Cancer Cell ◽  
Incubation Time ◽  
Gastric Cancer Cell ◽  
Gastric Cancer Cell Line ◽  
Cancer Cell Line ◽  
Root Extract ◽  
Human Gastric Cancer

Abstract One of the cancer-related deaths is gastric cancer in this area. Onosma dichroanthum Boiss. roots have been used as an antiseptic and anti-inflammatory for wound healing treatment. The aim of this study was to assess the in vitro cytotoxic and anticancer effects of O. dichroanthum Boiss. roots from the Golestan province of Iran. After identification of the taxonomical effect of O. dichroanthum Boiss., different concentrations of the hydroalcoholic root extract were used. Three different time periods (24, 48, and 72 h) were used to treat AGS gastric cancer and L-929 normal fibroblasts cell lines. The evaluation of different concentrations of root extract was performed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The 48 h treatment affected cell survival, while the concentration of 64 μg/mL was determined as IC50 concentrations at 48 h incubation time. The 48 h incubation time with 64 μg/mL showed the best effectiveness on cancerous cell-line while being safe for normal cell-line. Our results show that O. dichroanthum Boiss. roots extract may have cytotoxic and safe effects on gastric cancer cell-line and normal cells in 48 h treatment periods, respectively. The results indicated the O. dichroanthum Boiss. may be as an effective anticancer agent (gastric cancer).

Bombesin stimulates the in vitro growth of a human gastric cancer cell line

1994 ◽  
Vol 161 (3) ◽  
pp. 519-525 ◽  
Author(s):  
Richard J. Bold ◽  
Patrick S. Lowry ◽  
Jin Ishizuka ◽  
James F. Battey ◽  
Courtney M. Townsend ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Line ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Gastric Cancer Cell Line ◽  
Cancer Cell Line ◽  
Human Gastric Cancer ◽  
In Vitro Growth ◽  
Human Gastric Cancer Cell

scholarly journals Enhanced Vasculogenic Capacity Induced by 5-Fluorouracil Chemoresistance in a Gastric Cancer Cell Line

2021 ◽  
Vol 22 (14) ◽  
pp. 7698
Author(s):  
Sara Peri ◽  
Alessio Biagioni ◽  
Giampaolo Versienti ◽  
Elena Andreucci ◽  
Fabio Staderini ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Line ◽  
Cancer Cell ◽  
Intracellular Signaling ◽  
Gastric Cancer Cell ◽  
Gastric Cancer Cell Line ◽  
Cancer Cell Line ◽  
Tumor Evolution ◽  
Selective Growth Advantage

Chemotherapy is still widely used as a coadjutant in gastric cancer when surgery is not possible or in presence of metastasis. During tumor evolution, gatekeeper mutations provide a selective growth advantage to a subpopulation of cancer cells that become resistant to chemotherapy. When this phenomenon happens, patients experience tumor recurrence and treatment failure. Even if many chemoresistance mechanisms are known, such as expression of ATP-binding cassette (ABC) transporters, aldehyde dehydrogenase (ALDH1) activity and activation of peculiar intracellular signaling pathways, a common and universal marker for chemoresistant cancer cells has not been identified yet. In this study we subjected the gastric cancer cell line AGS to chronic exposure of 5-fluorouracil, cisplatin or paclitaxel, thus selecting cell subpopulations showing resistance to the different drugs. Such cells showed biological changes; among them, we observed that the acquired chemoresistance to 5-fluorouracil induced an endothelial-like phenotype and increased the capacity to form vessel-like structures. We identified the upregulation of thymidine phosphorylase (TYMP), which is one of the most commonly reported mutated genes leading to 5-fluorouracil resistance, as the cause of such enhanced vasculogenic ability.

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