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Published:
Aug 10, 2022DOI:
10.4314/tjpr.v21i6.6Keywords:
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Main Article Content
SLC6A14 promotes cell migration and inhibits autophagy in gastric cancer by regulating JAK2/STAT3 signaling
Abstract
Purpose: To investigate the role of solute carrier family 6-member 14 (SLC6A14) in gastric cancer (GC) tumorigenesis.
Methods: The GC cell proliferation was evaluated by CCK8 and colony formation assays. Flow cytometry and wound healing assays were used to investigate cell apoptosis and migration, respectively. Immunofluorescence was used to investigate autophagy.
Results: The SLC6A14 was elevated in GC cells (p < 0.001). Overexpression of SLC6A14 increased GC cell viability and migration (p < 0.001), increased colony formation, and suppressed cell apoptosis (p < 0.05). However, knockdown of SLC6A14 inhibited GC tumorigenesis by decreasing cell viability and migration, reducing colony formation, and promoting cell apoptosis (p < 0.001). Overexpression of SLC6A14 decreased the LC3-II/LC3-I ratio. Silencing of SLC6A14 increased the LC3-II/LC3-I ratio and increased the fluorescence intensity of LC3. Overexpression of SLC6A14 increased phosphorylation of JAK2 and STAT3 (p < 0.001).
Conclusion: Knockdown of SLC6A14 suppresses GC cell migration and proliferation and promotes autophagy through inactivation of JAK2/STAT3 signaling.
