Effect of Vitamin B12-conjugated Nanocomposite on Drug-resistant Gastric Cancer Cells

2021 ◽  
Vol 7 (5) ◽  
pp. 4244-4253
Author(s):  
Jiangshan Wu ◽  
Jian Liu ◽  
Xingwei Huang ◽  
Zhenping Wei ◽  
Yifei Zeng
Keyword(s):  
Gastric Cancer ◽  
Gastric Carcinoma ◽  
Vitamin B12 ◽  
Carcinoma Cells ◽  
Drug Resistant ◽  
Chitosan Derivative ◽  
Oral Drugs ◽  
Gastric Cancer Cells ◽  
New Type ◽  
Resistant Cells

Sericin nanomicelles (Sericin-PBLG) have the properties of efficiently and stably encapsulating hydrophobic chemotherapeutics in aqueous solution. The vitamin B12 (VB12) modified amphiphilic chitosan derivative can improve the delivery effect of oral drugs and has a targeting function. In this study, a new type of sericin nanomedicine (VB12-sericin-PBLG-PTX) loaded with paclitaxel was successfully synthesized. The particle size of VB12-sericin-PBLG-PTX nanomicelles is 121.5 ±1.6 nm. The nanomicelles can reduce the activity of gastric carcinoma cells and gastric carcinoma drug-resistant cells, and increase the apoptosis rate of gastric carcinoma cells and gastric carcinoma drug-resistant cells, and achieve a good anti-tumor effect.

scholarly journals TSPAN9 suppresses the chemosensitivity of gastric cancer to 5-fluorouracil by promoting autophagy

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Yaoyue Qi ◽  
Weiwei Qi ◽  
Shihai Liu ◽  
Libin Sun ◽  
Aiping Ding ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Transmembrane Protein ◽  
Pi3k Pathway ◽  
Drug Resistant ◽  
Gastric Cancer Cells ◽  
Autophagy Pathway ◽  
Resistant Cells

Abstract Background The issue of drug resistance in gastric cancer has attracted global attention. TSPAN9, a 4-transmembrane protein that plays an important role in tumor progression and signal transduction, has been found to be closely related to tumor invasion, metastasis, and autophagy. Methods Immunoblotting was used to evaluate TSPAN9 expression in parental and drug-resistant gastric cancer cells. Functional assays, such as the CCK-8 assay, were used to detect the proliferation of gastric cancer cells and the response of TSPAN9 to 5-fluorouracil (5-FU). Western blotting was used to analyze the expression of constituents of the PI3K/AKT/mTOR-mediated autophagy pathway induced by TSPAN9. Coimmunoprecipitation was performed to assess the specific mechanism by which TSPAN9 affects the PI3K pathway. Results We demonstrated that TSPAN9 is overexpressed in 5-FU-resistant cells compared to parental cells. 5-FU-mediated inhibition of cell proliferation can be significantly restored by increasing TSPAN9 expression, and inhibiting this expression in drug-resistant cells can restore the sensitivity of the cells to 5-FU. In addition, TSPAN9 also significantly promoted autophagy in gastric cancer cells in vitro. Further studies indicated that TSPAN9 downregulates the expression of PI3K and proteins associated with PI3K-mediated autophagy. In addition, TSPAN9 interacts with PI3K and inhibits its catalytic activity. Conclusion The current study reveals the important role of TSPAN9 in drug resistance to 5-FU in gastric cancer. It also provides a new target to clinically address drug-resistant gastric cancer and will contribute to the treatment strategy of this disease.

Dynamic characterization of drug resistance and heterogeneity of the gastric cancer cell BGC823 using single-cell Raman spectroscopy

The Analyst ◽  
2018 ◽  
Vol 143 (1) ◽  
pp. 164-174 ◽  
Author(s):  
Yong Zhang ◽  
Ludi Jin ◽  
Jingjing Xu ◽  
Yuezhou Yu ◽  
Lin Shen ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Raman Spectroscopy ◽  
Drug Resistance ◽  
Gastric Carcinoma ◽  
Single Cell ◽  
Gastric Cancer Cell ◽  
Carcinoma Cells ◽  
Dynamic Characterization ◽  
Human Gastric Carcinoma Cells

Drug resistance and heterogeneous characteristics of human gastric carcinoma cells (BGC823) under the treatment of paclitaxel (PTX) were investigated using single-cell Raman spectroscopy (RS).

Improvement of the Chemosensitivity of Gastric Carcinoma Cells by Celastrus orbiculatus Extracts

2021 ◽  
Vol 20 (2) ◽  
pp. 282-287
Author(s):  
Yuling Wang ◽  
Kai Wang ◽  
Shilei Ding ◽  
Shuguang Wang ◽  
Rubin Gu
Keyword(s):  
Gastric Carcinoma ◽  
Tumor Cells ◽  
Carcinoma Cells ◽  
High Morbidity ◽  
Drug Resistant ◽  
Celastrus Orbiculatus ◽  
Protein Markers ◽  
Gastric Cells ◽  
Human Gastric Carcinoma Cells ◽  
Selection Of

Gastric carcinoma is one of the most prevalent malignancies with high morbidity and mortality. While chemotherapy is the major means for the management gastric carcinoma, tumors gradually exhibit drug resistance. Therefore, there is a need for agents capable of enhancing the sensitivity of tumor cells to chemotherapy. Herein, we have examined the effect of Celastrus orbiculatus extracts on chemosensitivity of drug resistant gastric carcinoma cells. Human gastric carcinoma cells (MGC-803 and SGC-7901) were cultured in the presence of cisplatin for the selection of drug resistant gastric cells. Next, the effect of C. orbiculatus extracts on multiplication capacity of drug resistant MGC-803 and SGC-7901 cells was examined by a variety of measures. Following C. orbiculatus extract treatment, the multiplication and invasiveness of drug resistant MGC-803 and SGC-7901 cells declined remarkably, with increased apoptosis and decreased levels of β-catenin, c-Myc, and cyclin D1 proteins, protein markers critical to cell proliferation, differentiation, and apoptosis. In summary, C. orbiculatus extract can effectively improve the sensitivity of cisplatin resistant gastric carcinoma cells to cisplatin and promote the apoptosis of tumor cells through the inhibition of the expression of proteins associated with the Wnt/β-catenin axis.

Babao dan promotes apoptosis of cisplatin (DDP)-resistant gastric cancer cell line SGC-7901/DDP by inducing autophagy through PI3K/AKT/mTOR pathway modulation

2020 ◽  
Author(s):  
Jinyan Zhao ◽  
Weilan Lan ◽  
Jun Peng ◽  
Bin Guan ◽  
Jie Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Cell Line ◽  
Signaling Pathway ◽  
Caspase 3 ◽  
Mtor Pathway ◽  
Cell Protein ◽  
Drug Resistant ◽  
Gastric Cancer Cells

Abstract Background: Multidrug resistance (MDR) is a critical reason of cancer chemotherapy failure. Babao dan (BBD) is a classical and famous traditional Chinese patent medicine, which has been reported to has anti-gastric cancer activity. However, the roles and molecular mechanisms of the reversal of MDR of gastric cancer by BBD have not been well described until now. Methods: SGC-7901 and SGC-7901/DDP cells were used in this study, and drug resistance and evaluation of the reversal effect of BBD was determined using MTT assays in SGC7901/DDP cells. Doxorubicin (DOX) and Rhodamin123 (Rho123) staining was performed to assess BBD effects on drug accumulation and efflux of drug-resistant gastric cancer cells. Cell apoptosis was directly assessed using DAPI staining. Apoptotic and dead cells were detected by flow cytometry after staining with Annexin V-FITC and propidium iodide (PI). Cyto-ID assays were performed to examine cellular autophagy. Changes in cell protein expression of ABCB1, ABCC1, ABCG2, Bax, Bcl-2, caspase-3, cleaved-caspase-3, LC3, p62, Beclin1 and the PI3K/AKT/mTOR pathway were detected by Western blot. Inhibition of autophagy with 3-MA, chloroquine (CQ) and PI3K antagonist (LY294002) or agonist (740Y-P) , uncovered a role for the potentially downregulated signaling pathway, PI3K/AKT/mTOR.Results: The SGC7901/DDP cell line exhibited multi-drug resistance to DDP, DOX and 5-fluorouracil (5-FU) and the drug resistant index (RI) of DDP, DOX and 5-FU were 1.86, 1.50 and 47.70, respectively. BBD reversed the MDR of SGC7901/DDP cells by increasingDOX accumulation, reducing Rh123 efflux and down-regulating the expression of ABCB1, ABCC1, ABCG2. Furthermore, BBD induced apoptosis in SGC7901/DDP cells through regulating caspase-3, cleaved-caspase-3, Bax and Bcl-2. Moreover, BBD induced autophagy in DDP-resistant gastric cancer cells via regulating p62, LC3 and Beclin1. Pathway analyses suggested BBD may inhibit PI3K/AKT/mTOR pathway activity and subsequent autophagy induction. Conclusions: BBD may reverse the MDR of gastric cancer cells, and promote autophagic death via inactivation of the PI3K/AKT/mTOR signaling pathway.

Calebin-A induces apoptosis and modulates MAPK family activity in drug resistant human gastric cancer cells

2008 ◽  
Vol 591 (1-3) ◽  
pp. 252-258 ◽  
Author(s):  
Yan Li ◽  
Shaoqing Li ◽  
Yueheng Han ◽  
Junye Liu ◽  
Jian Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Human Gastric Cancer ◽  
Drug Resistant ◽  
Gastric Cancer Cells ◽  
Family Activity

Mitotic Catastrophe Induced by Chelidonine on Human Gastric Carcinoma SGC-7901 Cells

2013 ◽  
Vol 790 ◽  
pp. 562-565
Author(s):  
Zhong Yuan Qu ◽  
Xiang Zou ◽  
Jing Wen Zhao ◽  
Yu Bin Ji
Keyword(s):  
Gastric Carcinoma ◽  
Mitotic Index ◽  
Morphological Changes ◽  
Giant Cells ◽  
Carcinoma Cells ◽  
Mitotic Catastrophe ◽  
Control Group ◽  
Induction Effect ◽  
Gastric Cancer Cells ◽  
Human Gastric Carcinoma

To study the mitotic catastrophe induction effect of chelidonine on human gastric carcinoma SGC-7901 cells, MTT assay was applied to detect the proliferation inhibition effect of chelidonine. Giemsa staining was used to observe the morphological changes of the nucleus in gastric cancer cells and mitotic index (MI) was calculated. The results showed that chelidonine could effectively inhibit the proliferation of SGC-7901 cells and the IC50 was 48.67μmol/L. After treatment with 6.25-25μmol/L chelidonine, the numbers of giant cells with two or more nuclei was increased along with the increase of drug concentration. The mitotic index of cells was significantly increased compared with that of the control group (P<0.01). The conclusion can be drawn that chelidonine can inhibit the proliferation of SGC-7901 cells by inducing mitotic catastrophe of gastric carcinoma cells.

A novel K-samII/FGF-R2 autophosphorylation inhibitor is therapeutically useful for scirrhous gastric carcinoma with K-samII amplification

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 14070-14070
Author(s):  
M. Yashiro ◽  
K. Nakamura ◽  
T. Sawada ◽  
H. Kawajiri ◽  
T. Shimizu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Growth Factor ◽  
Gastric Carcinoma ◽  
Cancer Cells ◽  
Peritoneal Dissemination ◽  
Growth Factor Receptor ◽  
Carcinoma Cells ◽  
Apoptosis Pathway ◽  
Scirrhous Gastric Cancer ◽  
Scirrhous Gastric Carcinoma

14070 Background: Scirrhous gastric carcinoma, a diffusely infiltrating also known as linitis plastica-type carcinoma, carries the highest mortality of all gastric cancers. Scirrhous carcinoma cells with amplification of the activated K-samII gene, which encodes fibroblast growth factor receptor type 2 (FGF-R2), have a growth advantage during tumor progression The poor prognosis carried by scirrhous gastric cancer is closely associated with amplification of the K-samII/FGF-R2, a tyrosine kinase growth factor receptor. Ki23057, a newly developed small molecule acting K-samII/FGF-R2 inhibitor, is a kinase inhibitor that competes with ATP for the binding site in the kinase, thus strongly blocking phosphorylation of FGF-R2. The aim of the current study is to clarify the possibility of molecular target therapy with Ki23057 for treating scirrhous gastric cancer. Methods: Five human gastric cancer cell lines were used. OCUM-2MD3 and OCUM-8 were derived from scirrhous carcinomas. MKN-7, MKN-45 and MKN-74 cells were derived from non-scirrhous carcinomas. In vitro effects of Ki23057 on cell growth were determined by calculating the number of cancer cells. The influences of Ki23057 on the MAP kinase and PI3 kinase signaling pathways and the apoptosis pathway in the gastric cancer cells were also examined. For in vivo experiments, the Ki23057 was administered orally to mouse models of peritoneal dissemination. Results: K-samII amplification was found in OCUM-2MD3 and OCUM-8 cells, but not in MKN-7, MKN-45, or MKN-74 cells. Ki23057 significantly inhibited the proliferation of scirrhous cancer cells, but not non- scirrhous gastric carcinoma cells. Ki23057 decreased phosphorylation of K-samII/FGF-R2, ERK and Akt, and increased apoptosis in scirrhous cancer lines. The oral Ki23057 administration significantly (p<0.001) prolonged survival of mice with peritoneal dissemination following injection of OCUM-2MD3 scirrhous cancer cells. Conclusions: A novel K-samII/FGF-R2 phosphorylation inhibitor, Ki23057, appears therapeutically promising in scirrhous gastric carcinoma with K-samII amplification. No significant financial relationships to disclose.

Chrysin Alters microRNAs Expression Levels in Gastric Cancer Cells: Possible Molecular Mechanism

Drug Research ◽  
2017 ◽  
Vol 67 (09) ◽  
pp. 509-514 ◽  
Author(s):  
Farideh Mohammadian ◽  
Younes Pilehvar-Soltanahmadi ◽  
Shahriar Alipour ◽  
Mehdi Dadashpour ◽  
Nosratollah Zarghami
Keyword(s):  
Gastric Cancer ◽  
Gastric Carcinoma ◽  
Cancer Cells ◽  
Molecular Mechanism ◽  
Molecular Mechanisms ◽  
Gastric Cancer Cells ◽  
Gastric Carcinoma Cell ◽  
Expression Levels ◽  
Mirnas Expression ◽  
Chemopreventive Activity

Abstract Background Gastric carcinoma still remains the second most common cause of cancer mortality in the world. Chrysin, as a flavone, has showed cancer chemopreventive activity. The cellular and molecular mechanisms of chrysin in cancer cells have not been fully understood. Objective In this study, we investigate expression levels of let-7a, miR-9, mir-18a, miR-21, miR-22, miR-34a, miR-126 and mir-221 to describe the anti-cancer effects of chrysin. Materials and Methods The cytotoxic effects of chrysin were assessed using MTT assay. The effect of chrysin on the microRNAs expression was determined by qRT-PCR. Results The MTT results for different concentrations of chrysin at different times on the Gastric carcinoma cells showed that IC50 for chrysin was 68.24 µM after 24 h of treatment. Expression analysis identified that miR-18, miR-21 and miR-221 were down regulated whereas let-7a, miR-9, miR-22, miR-34a and miR-126 were up regulated in Gastric carcinoma cell line (p<0.05). Conclusion Treatment with chrysin can alter the miRNAs expression and these findings might be an explanation for molecular mechanism of chrysin effect on gastric cancer.

A FGFR2 inhibitor, Ki23057, enhances the chemosensitivity of drug-resistant gastric cancer cells

2011 ◽  
Vol 307 (1) ◽  
pp. 47-52 ◽  
Author(s):  
Hong Qiu ◽  
Masakazu Yashiro ◽  
Xiaotian Zhang ◽  
Atsushi Miwa ◽  
Kosei Hirakawa
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Drug Resistant ◽  
Gastric Cancer Cells
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