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The Elevated ASK1 Expression Inhibits Proliferation and Invasion in Gastric Cancer HGC-27 Cells
Xiaochen Wan1, Liying Shi1, Xiaohong Ma1
1Department of Clinical Laboratory, Zhejiang Hospital, Hangzhou, 310013, People's Republic of China.
Abstract:
This study aimed to evaluate the effects and mechanism of action of ASK1 gene on the growth and migration of gastric cancer (GC) cells. Total RNA was extracted from the gastric cell lines and GC tissues. The expression level of ASK1, and the association between ASK1 expression and clinicopathological characteristics was assessed by real-time polymerase chain reaction. The effects of ASK1 on the proliferation of HGC-27 cells were assessed by the CCK-8 assay. In addition, the effects of ASK1 on the migration of HGC-27 cells were analyzed by the migration assay using transwell chambers. The expression levels of signaling proteins related to cell migration were detected by Western blotting. Although no significant differences were observed in the expression levels of ASK1 between the GC tissue samples and the normal tissue samples (P = 0.241), ASK1 expression correlated with tumor lymph node metastasis (P = 0.008). Furthermore, ASK1 inhibited proliferation and migration of HGC-27 cells. The increase in the expression of ASK1 in HGC-27 cells induced the activation of the JNK and p38 signaling pathways. The findings demonstrated that increased ASK1 expression level inhibited migration and proliferation of HGC-27 gastric cancer cells, whereas the possible mechanism of action may be attributed to the activation of the JNK and p38 signaling pathways. Anat Rec, 301:1815-1819, 2018. © 2018 Wiley Periodicals, Inc.
Insights
Increased ASK1 gene expression inhibits gastric cancer cell growth and migration. This occurs through the activation of the JNK and p38 signaling pathways, suggesting ASK1 as a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Gastric cancer (GC) remains a significant global health challenge.
- Understanding the molecular mechanisms regulating GC cell growth and metastasis is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role and mechanism of action of the ASK1 gene in gastric cancer cell proliferation and migration.
- To explore the association between ASK1 expression and clinicopathological features of GC.
Main Methods:
- Real-time PCR was used to assess ASK1 gene expression in GC cell lines and tissues.
- CCK-8 and transwell assays were employed to evaluate the effects of ASK1 on HGC-27 cell proliferation and migration.
- Western blotting was utilized to detect the expression of key signaling proteins.
Main Results:
- ASK1 expression did not significantly differ between GC tissues and normal tissues but correlated with lymph node metastasis (P = 0.008).
- Elevated ASK1 expression inhibited proliferation and migration of HGC-27 cells.
- Increased ASK1 expression activated the JNK and p38 signaling pathways.
Conclusions:
- Increased ASK1 expression suppresses gastric cancer cell proliferation and migration.
- The mechanism involves the activation of the JNK and p38 signaling pathways.
- ASK1 may represent a potential therapeutic target for gastric cancer.
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