Inhibition of Vav3 could reverse the drug resistance of gastric cancer cells by downregulating JNK signaling pathway

To investigate the impact of miRNA-206 on the transcriptional expression of EVI1 gene and activation of Akt/JNK signaling pathway in gastric cancer cells, and to provide a new idea for gene-targeted therapy of gastric cancer. The miRNA-206 transfection experiment was firstly used to verify the regulation of EVI1. The experiment was divided into three groups: miRNA-206 mimics (100 nM), miRNA-206 inhibitor (100 nM), miR-NC (100 nM), and transfected into gastric cancer cells sgc7901, Western blot. EVI1 protein expression was detected; then the signal transduction and biological behavior of the cells were verified by miRNA-206 lentiviral vector transfection experiments. The experiment was divided into three groups: pLB-miRNA-206 group, empty vector group and control group (sgc7901 cell group). miRNA-206 and EVI1 mRNA levels were detected by real-time fluorescence quantitative (RT-PCR), and p-Akt and p-JNK were detected by Western blot. Protein expression, cell proliferation was quantified by MTT assay, and the alteration of cell cycle were detected by flow cytometry. miRNA-206 may affect the cell proliferation and division cycle by targeting the regulation of EVI1 transcriptional gene expression and activation of Akt/JNK signaling pathway in gastric cancer cells, and it is expected to provide an important selection site for gene-targeted therapy of gastric cancer.

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Schisantherin A induces cell apoptosis through ROS/JNK signaling pathway in human gastric cancer cells

Biochemical Pharmacology ◽

10.1016/j.bcp.2019.113673 ◽

2020 ◽

Vol 173 ◽

pp. 113673 ◽

Cited By ~ 4

Author(s):

Zishu Wang ◽

Kaikai Yu ◽

Yudong Hu ◽

Fang Su ◽

Zhenyuan Gao ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Signaling Pathway ◽

Cell Apoptosis ◽

Human Gastric Cancer ◽

Gastric Cancer Cells ◽

Jnk Signaling ◽

Jnk Signaling Pathway ◽

Schisantherin A

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XEDAR inhibits the proliferation and induces apoptosis of gastric cancer cells by regulating JNK signaling pathway

Bioscience Reports ◽

10.1042/bsr20192726 ◽

2019 ◽

Vol 39 (12) ◽

Author(s):

Lihong Yang ◽

Xiaojun Huang ◽

Wei Wang ◽

Tao Jiang ◽

Feifei Ding

Keyword(s):

Gastric Cancer ◽

Cell Proliferation ◽

Cancer Cells ◽

Signaling Pathway ◽

Molecular Mechanisms ◽

Gastric Cancer Cells ◽

Jnk Signaling ◽

Jnk Signaling Pathway ◽

Induced Apoptosis ◽

Cancer Tissues

Abstract X-linked ectodermal dysplasia receptor (XEDAR) has been widely studied in epidermal morphogenesis, but few studies have been conducted on tumorigenesis and development, including gastric cancer. In the present research, we aimed to investigate the effect of XEDAR on gastric cancer and further explore the molecular mechanisms involved. The differential expression of XEDAR in 90 tissue specimens (30 gastric cancer tissues, 30 adjacent tissues and 30 normal tissues) was detected by real-time PCR (RT-PCR) and Western blot. Cell proliferation and apoptosis were explored using MTT and Annexin-V/propidium iodide (PI) assays, respectively. The results revealed that the expression of XEDAR was decreased in gastric cancer tissues and in gastric cancer cell lines, and its expression is regulated by p53 in BGC-823 cells. Furthermore, overexpression of XEDAR inhibited cell proliferation and induced apoptosis in BGC-823 cells. XEDAR moreover inhibited proliferation and induced apoptosis in gastric cancer cells by regulating the JNK signaling pathway. Collectively, the results of the present study suggested that XEDAR inhibits cell proliferation and induces apoptosis by participating in p53-mediated signaling pathway and inhibiting the downstream JNK signaling pathway in gastric cancer.

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GREM2 maintains stem cell-like phenotypes in gastric cancer cells by regulating the JNK signaling pathway

Cell Cycle ◽

10.1080/15384101.2019.1646561 ◽

2019 ◽

Vol 18 (19) ◽

pp. 2414-2431 ◽

Cited By ~ 2

Author(s):

Ao Ran ◽

Lin Guan ◽

Jiani Wang ◽

Ying Wang

Keyword(s):

Gastric Cancer ◽

Stem Cell ◽

Cancer Cells ◽

Signaling Pathway ◽

Gastric Cancer Cells ◽

Jnk Signaling ◽

Jnk Signaling Pathway

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Sanguinarine inhibits the proliferation of BGC-823 gastric cancer cells via regulating miR-96-5p/miR-29c-3p and the MAPK/JNK signaling pathway

Journal of Natural Medicines ◽

10.1007/s11418-019-01330-7 ◽

2019 ◽

Vol 73 (4) ◽

pp. 777-788 ◽

Cited By ~ 8

Author(s):

Xian-Zhe Dong ◽

Yan Song ◽

Yu-Pan Lu ◽

Yuan Hu ◽

Ping Liu ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Signaling Pathway ◽

Gastric Cancer Cells ◽

Jnk Signaling ◽

Jnk Signaling Pathway

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

10.21203/rs.3.rs-110952/v1 ◽

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.

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