Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

SLC6A14 promotes cell migration and inhibits autophagy in gastric cancer by regulating JAK2/STAT3 signaling

Haifeng Wang¹, Jindao Wang²

¹Department of Gastrointestinal Surgery, Shaoxing People's Hospital, Shaoxing, Zhejiang Province 312000, China; ²Department of Endoscopy Center, Shaoxing People's Hospital, Shaoxing, Zhejiang Province 312000, China.

For correspondence:- Jindao Wang Email: Wangjindao_666@163.com Tel:+8657588558602

Accepted: 24 May 2022 Published: 30 June 2022

Citation: Wang H, Wang J. SLC6A14 promotes cell migration and inhibits autophagy in gastric cancer by regulating JAK2/STAT3 signaling. Trop J Pharm Res 2022; 21(6):1177-1182 doi: 10.4314/tjpr.v21i6.6

© 2022 The authors.
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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.

Keywords: SLC6A14, Gastric cancer, Proliferation, Migration, Autophagy, JAK2/STAT3