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Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion
Published on: April 2, 2020
Knockdown of ARK5 Expression Suppresses Invasion and Metastasis of Gastric Cancer
Background/Aims:
Gastric cancer (GC) is a common and lethal malignancy, and AMP-activated protein kinase-related kinase 5 (ARK5) has been discovered to promote cancer metastasis in certain types of cancer. In this study, we explored the role of ARK5 in GC invasion and metastasis.
Methods:
ARK5 and epithelial-mesenchymal transition (EMT)-related markers were determined by immunohistochemistry and western blot in GC specimens. Other methods including stably transfected against ARK5 into SGC7901 and AGS cells, western blot, migration and invasion assays in vitro and nude mice tumorigenicity in vivo were also employed.
Results:
The results demonstrated that ARK5 expression was increased and positively correlated with metastasis, EMT-related markers and poor prognosis in patients with GC. Knockdown of ARK5 expression remarkably suppressed GC cells invasion and metastasis via regulating EMT, rather than proliferation in vitro and in vivo. And knockdown of ARK5 expression in GC cells resulted in the down-regulation of the mTOR/p70S6k signals, Slug and SIP1.
Conclusion:
The elevated ARK5 expression was closely associated with cancer metastasis and patient survival, and it seemed to function in GC cells migration and invasion via EMT alteration, together with the alteration of the mTOR/p70S6k signals, Slug and SIP1, thus providing a potential therapeutic target for GC.
Insights
AMP-activated protein kinase-related kinase 5 (ARK5) promotes gastric cancer (GC) metastasis. Inhibiting ARK5 suppressed GC cell invasion and metastasis by regulating epithelial-mesenchymal transition (EMT), offering a potential therapeutic target for GC.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Gastric cancer (GC) is a significant cause of cancer-related mortality.
- AMP-activated protein kinase-related kinase 5 (ARK5) is implicated in promoting metastasis in various cancers.
Purpose of the Study:
- To investigate the role of ARK5 in gastric cancer (GC) invasion and metastasis.
- To explore ARK5 as a potential therapeutic target for GC.
Main Methods:
- Immunohistochemistry and western blot to assess ARK5 and epithelial-mesenchymal transition (EMT) markers in GC specimens.
- In vitro assays (cell transfection, migration, invasion) and in vivo nude mice tumorigenicity studies were performed.
- Analysis of downstream signaling pathways including mTOR/p70S6k, Slug, and SIP1.
Main Results:
- Elevated ARK5 expression correlates with increased metastasis, EMT markers, and poorer prognosis in GC patients.
- ARK5 knockdown significantly inhibited GC cell invasion and metastasis in vitro and in vivo.
- ARK5 inhibition led to the downregulation of mTOR/p70S6k signaling, Slug, and SIP1, suggesting EMT regulation.
Conclusions:
- Increased ARK5 expression is linked to gastric cancer metastasis and reduced patient survival.
- ARK5 appears to drive GC cell migration and invasion through EMT modulation and downstream signaling.
- ARK5 represents a promising therapeutic target for combating gastric cancer metastasis.
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