DcR3 induces proliferation, migration, invasion, and EMT in gastric cancer cells via the PI3K/AKT/GSK-3β/β-catenin signaling pathway

Abstract Background Recently, tRNA-derived fragments (tRFs) have been shown to serve important biological functions. However, the role of tRFs in gastric cancer has not been fully elucidated. This study aimed to identify the tumor suppressor role of tRF-5026a (tRF-18-79MP9P04) in gastric cancer. Methods Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was first used to detect tRF-5026a expression levels in gastric cancer tissues and patient plasma. Next, the relationship between tRF-5026a levels and clinicopathological features in gastric cancer patients was assessed. Cell lines with varying tRF-5026a levels were assessed by measuring tRF-5026a using qRT-PCR. After transfecting cell lines with a tRF-5026a mimic or inhibitor, cell proliferation, colony formation, migration, apoptosis, and cell cycle were evaluated. The expression levels of related proteins in the PTEN/PI3K/AKT pathway were also analyzed by Western blotting. Finally, the effect of tRF-5026a on tumor growth was tested using subcutaneous tumor models in nude mice. Results tRF-5026a was downregulated in gastric cancer patient tissues and plasma samples. tRF-5026a levels were closely related to tumor size, had a certain diagnostic value, and could be used to predict overall survival. tRF-5026a was also downregulated in gastric cancer cell lines. tRF-5026a inhibited the proliferation, migration, and cell cycle progression of gastric cancer cells by regulating the PTEN/PI3K/AKT signaling pathway. Animal experiments showed that upregulation of tRF-5026a effectively inhibited tumor growth. Conclusions tRF-5026a (tRF-18-79MP9P04) is a promising biomarker for gastric cancer diagnostics and has tumor suppressor effects mediated through the PTEN/PI3K/AKT signaling pathway.

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

Cancer Gene Therapy ◽

10.1038/cgt.2014.59 ◽

2014 ◽

Vol 21 (12) ◽

pp. 526-531 ◽

Cited By ~ 5

Author(s):

B Tan ◽

Y Li ◽

Q Zhao ◽

L Fan ◽

Y Liu ◽

...

Keyword(s):

Gastric Cancer ◽

Drug Resistance ◽

Cancer Cells ◽

Signaling Pathway ◽

Gastric Cancer Cells ◽

Jnk Signaling ◽

Jnk Signaling Pathway

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Netrin‑1 induces the proliferation of gastric cancer cells via the ERK/MAPK signaling pathway and FAK activation

Oncology Reports ◽

10.3892/or.2018.6614 ◽

2018 ◽

Cited By ~ 1

Author(s):

Kai Yin ◽

Mengyuan Shang ◽

Shengchun Dang ◽

Linjun Wang ◽

Yiwen Xia ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Signaling Pathway ◽

Mapk Signaling ◽

Mapk Signaling Pathway ◽

Gastric Cancer Cells ◽

Erk Mapk

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Apelin Over-Expression Promotes Proliferation and Angiogenesis of Gastric Cancer Cells

10.21203/rs.3.rs-530677/v2 ◽

2021 ◽

Author(s):

Li-Jun Tian ◽

Hong-Zhi Liu ◽

Qiang Zhang ◽

Dian-Zhong Geng ◽

Jing Yang ◽

...

Keyword(s):

Gastric Cancer ◽

Cyclin D1 ◽

Cancer Cells ◽

Signaling Pathway ◽

Cox Regression ◽

Gastric Cancer Cells ◽

Over Expression ◽

Normal Tissues

Abstract Background: Apelin is a recently identified endogenous ligand associated with proliferation and angiogenesis of several cancers. However, only few studies have reported on the functions and the role of apelin in gastric cancer (GC). Therefore, in the present study, we investigated the association and the mechanisms underlying Apelin expression and proliferation of GC cells both in vitro and in vivo.Methods: We enrolled 178 postoperative care GC patients to investigate clinicopathological and immunohistochemical factors associated with Apelin expression. The relationship between Survival of patients and apelin expression was evaluated using Kaplan-Meier method and Cox regression analyses. The expression of apelin mRNA and its proteins in GC tissues and cell lines were analyzed using quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR), western blot and ELISA. The role and mechanisms underlying regulation of Apelin expression in human GC cells were evaluated through several in vitro and in vivo experiments. Results: Apelin was over expressed in human GC cells, relative to adjacent normal tissues. The over expression of apelin was associated with vessel invasion (P <0.01), lymph node metastasis (P <0.01), late-staged tumor (T) (P <0.05), worse pathological type (P <0.05), nerve invasion (P <0.05). In addition, expression of apelin strongly and positively correlated with that of vascular endothelial growth factor (VEGF). Over-expression of apelin promoted proliferation and invasion of MGC-803 cell via the ERK/Cyclin D1/MMP-9 signaling pathway. Apelin over-expression also promoted angiogenesis of GC cells, accelerating growth of subcutaneous xenograft of the cancer cells in vivo.Conclusions: Over-expression of apelin promotes proliferation and metastasis of GC cells via the ERK/Cyclin D1/MMP-9 signaling pathway and is associated with adverse events of the cancer. Consequently, apelin is a potential therapeutic target for human GC.

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Downregulation of FABP5 Suppresses the Proliferation and Induces the Apoptosis of Gastric Cancer Cells Through the Hippo Signaling Pathway

DNA and Cell Biology ◽

10.1089/dna.2021.0370 ◽

2021 ◽

Author(s):

Wendong Wang ◽

Zhenzhen Liu ◽

Xin Chen ◽

Yongqu Lu ◽

Bingyan Wang ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Signaling Pathway ◽

Hippo Signaling ◽

Gastric Cancer Cells ◽

Hippo Signaling Pathway

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Effects of Amygdalin on TLR4/NF-αB Signaling Pathway-Mediated Proliferation and Apoptosis of Gastric Cancer Cells

Current Topics in Nutraceutical Research ◽

10.37290/ctnr2641-452x.20:153-158 ◽

2021 ◽

Vol 20 (1) ◽

pp. 153-158

Author(s):

Abulajiang Abudoukelimu ◽

Xinhui Yang ◽

Lei Ge ◽

Xiangyue Zeng ◽

Yin Shu ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Signaling Pathway ◽

B Cell Lymphoma ◽

Toll Like Receptor ◽

Gastric Cancer Cells ◽

Toll Like Receptor 4 ◽

Proliferation And Apoptosis ◽

High Incidence Rate ◽

Factor Α

Gastric cancer is a highly malignant tumor of the digestive tract with high incidence rate and mortality. In the present study, we have shown decreased cell proliferation, increased apoptosis, and expression of proinflammatory cytokines (Interleukin-6, Interleukin-1β, and Tumor necrosis factor-α) in gastric cancer cells MGC-803 by amygdalin. Also, amygdalin treatment significantly reduced expression of the mRNA and protein for B-cell lymphoma 2 protein, CyclinD1, toll-like receptor 4, and REL-associated protein involved in NF-κB heterodimer formation in MGC-803 cells. In summary, amygdalin inhibits the proliferation of gastric cancer cells MGC-803 and promotes cell apoptosis by regulating the toll-like receptor 4/ nuclear factor-kappa B 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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