Dihydromyricetin induces cell apoptosis via a p53-related pathway in AGS human gastric cancer cells

Gastric cancer is one of the most fatal diseases around the world. However, the mechanism of the development of gastric cancer is still not clarified. In addition, the anticancer drugs have cytotoxicity with different degrees. AnnexinA5, a member of the annexin family, has a great binding ability with the membrane phospholipid in a calcium dependent manner and is involved in the development of various cancers. This study aims to explore the influence of annexinA5 on human gastric cancer cells and whether it has the potential to be an auxiliary treatment to gastric cancer. In this study, the role of annexinA5 was detected from both the endogenous and the exogenous aspects on the gastric cancer cell lines MGC-803 and MKN-45. The cells were divided into a knockdown group in which RNA interference technique was used to suppress annexinA5 expression and a protein-supplementing group in which annexinA5 protein was added in the culture supernatant. After the suppression ratio of RNA interference was determined and the IC50 of annexinA5 protein was decided respectively, the cells’ proliferation was detected by MTT assay, colony formation assay, and the expression of PCNA. FCM assay and PI staining methods were applied to test cell apoptosis and necrosis. To investigate whether ANXA5 influence cell metastasis, wound healing assay and transwell assay were employed. To further detect the mechanism of annexinA5 action, the signal pathway was examined with Western Blot method. When ANXA5 gene was knocked down, cell proliferation and metastasis were promoted, while cell apoptosis was suppressed. On the other hand, after the annexinA5 protein was applied to the gastric cancer cells, cell proliferation and metastasis were inhibited, while cell apoptosis and necrosis were promoted. AnnexinA5 played its role via ERK signal pathway. ANXA5 acted as tumor suppressor gene in the gastric cancer by suppressing ERK signal pathway and has the potentiality to be an auxiliary anticancer agent.

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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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Quercetin induced cell apoptosis and altered gene expression in AGS human gastric cancer cells

Environmental Toxicology ◽

10.1002/tox.22623 ◽

2018 ◽

Vol 33 (11) ◽

pp. 1168-1181 ◽

Cited By ~ 10

Author(s):

Hung-Sheng Shang ◽

Hsu-Feng Lu ◽

Ching-Hsiao Lee ◽

Han-Sun Chiang ◽

Yung-Lin Chu ◽

...

Keyword(s):

Gene Expression ◽

Gastric Cancer ◽

Cancer Cells ◽

Cell Apoptosis ◽

Human Gastric Cancer ◽

Gastric Cancer Cells ◽

Altered Gene Expression ◽

Altered Gene

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The p62/Keap1/Nrf2 axis in the control of C-2 induced human gastric cancer cell death switching between autophagy and apoptosis

10.21203/rs.3.rs-147863/v1 ◽

2021 ◽

Author(s):

ZhenYa Wang ◽

Yong Guo ◽

En Zhang ◽

QianHong Ban ◽

MengLin Wang ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Cell Apoptosis ◽

Target Genes ◽

Beclin 1 ◽

Human Gastric Cancer ◽

Gastric Cancer Cells ◽

Compound C ◽

Anti Cancer ◽

Cancer Activity

Abstract Background Compound C-2 is a derivative of natural product Jaspine B and possesses anti-cancer activity against bladder cancer cells. However, little is known about its anti-cancer activity against gastric cancer. In this research, mechanism underlying anti-cancer effect of C-2 in gastric cancer cells was well investigated. Methods Anti-cancer activities of C-2 were determined by MTT, western blotting and flow cytometry. A serial of specific inhibitors, immunoprecipitation, siRNA and immunofluorescence were utilized to explore signaling pathways affected by C-2. Results C-2 induces apoptosis in gastric cancer cells through the internal mitochondrial pathway, and triggers autophagy in gastric cancer cells through JNK/ERK pathway. Phosphorylated JNK/ERK further activates Beclin1 via disturbing Beclin-1/Bcl-xL or Beclin-1/Bcl-2 complexes, leading to autophagy and up-regulated p62. Next, p62 competitively binds keap1 to release Nrf2, thus promoting translocation of Nrf2 from cytoplasm to nucleus and triggering expression of Nrf2 target genes. Pharmacological inhibition or knockdown of key proteins in autophagy attenuates C-2 induced cell apoptosis, indicating that autophagy antagonizes cell apoptosis induced by C-2. Conclusion C-2 possesses anti-tumor activity against gastric cancer cells, while C-2 triggered-autophagy antagonizes cell arrest and apoptosis induced by C-2 by upregulating Nrf2 in nucleus.

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Blockade of cholecystokinin-2 receptor and cyclooxygenase-2 synergistically induces cell apoptosis, and inhibits the proliferation of human gastric cancer cells in vitro

Cancer Letters ◽

10.1016/j.canlet.2008.01.012 ◽

2008 ◽

Vol 263 (2) ◽

pp. 302-311 ◽

Cited By ~ 38

Author(s):

Wei-Hao Sun ◽

Feng Zhu ◽

Guo-Sheng Chen ◽

Han Su ◽

Cheng Luo ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Cell Apoptosis ◽

Cyclooxygenase 2 ◽

Human Gastric Cancer ◽

Gastric Cancer Cells

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LncRNA UCA1 promotes development of gastric cancer via the miR-145/MYO6 axis

Cellular & Molecular Biology Letters ◽

10.1186/s11658-021-00275-8 ◽

2021 ◽

Vol 26 (1) ◽

Author(s):

An Yang ◽

Xin Liu ◽

Ping Liu ◽

Yunzhang Feng ◽

Hongbo Liu ◽

...

Keyword(s):

Gastric Cancer ◽

Cell Proliferation ◽

Cancer Cells ◽

Cell Apoptosis ◽

Gastric Cancer Cell ◽

Gastric Cancer Cells ◽

Gastric Cancer Cell Lines ◽

Development Of Gastric Cancer

Abstract Background Long noncoding RNA (lncRNA), urothelial carcinoma-associated 1 (UCA1) is aberrantly expressed in multiple cancers and has been verified as an oncogene. However, the underlying mechanism of UCA1 in the development of gastric cancer is not fully understood. In the present study, we aimed to identify how UCA1 promotes gastric cancer development. Methods The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) data were used to analyze UCA1 and myosin VI (MYO6) expression in gastric cancer. Western blot and quantitative real-time PCR (QPCR) were performed to test the expression level of the UCA1/miR-145/MYO6 axis in gastric cancer cell lines and tissues. The roles of the UCA1/miR-145/MYO6 axis in gastric cancer in vitro and in vivo were investigated by CCK-8 assay, flow cytometry, siRNAs, immunohistochemistry, and a mouse xenograft model. The targeted relationship among UCA1, miR-145, and MYO6 was predicted using LncBase Predicted v.2 and TargetScan online software, and then verified by luciferase activity assay and RNA immunoprecipitation. Results UCA1 expression was higher but miR-145 expression was lower in gastric cancer cell lines or tissues, compared to the adjacent normal cell line or normal tissues. Function analysis verified that UCA1 promoted cell proliferation and inhibited cell apoptosis in the gastric cancer cells in vitro and in vivo. Mechanistically, UCA1 could bind directly to miR-145, and MYO6 was found to be a downstream target gene of miR-145. miR-145 mimics or MYO6 siRNAs could partly reverse the effect of UCA1 on gastric cancer cells. Conclusions UCA1 accelerated cell proliferation and inhibited cell apoptosis through sponging miR-145 to upregulate MYO6 expression in gastric cancer, indicating that the UCA1/miR-145/MYO6 axis may serve as a potential therapeutic target for gastric cancer.

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