<p>Gastric cancer is a significant contributor to worldwide cancer deaths with limited treatment options and poor patient survival. MicroRNAs play crucial roles as potential oncogenic factors or tumor suppressors in cancers by modulating cell cycle progression, proliferation, migration, invasion, and apoptosis. However, the functional implications of miR-103a-3p in gastric cancer remain poorly known. The current study demonstrates a noteworthy increase in the expression of miR-103a-3p in gastric cancer tissues when compared to neighboring non-cancerous tissues. Our functional investigations indicate that the upregulation of miR-103a-3p contributes to enhanced proliferation, invasion, and migration capabilities in gastric cancer cells. After mechanistic studies, our findings indicate that miR-103a-3p may directly target insulin-like growth factor binding protein 5 (IGFBP5) in gastric cancer. Moreover, rescue experiments reveal that IGFBP5 overexpression can attenuate the progression induced by miR-103a-3p in gastric cancer cells. In summary, our findings suggest that the miR-103a-3p/IGFBP5 axis may play a role in gastric cancer progression, highlighting its potential as a therapeutic target and prognostic marker.</p>

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Targeting miR-103a-3p/IGFBP5 axis: a potential therapeutic strategy for gastric cancer progression

  • Junrui Zhang,
  • Yue Qiu,
  • Fubin Ma,
  • Xingdong Niu,
  • Pengwei Bai,
  • Mingxu Da,
  • Junfeng Ma

摘要

Gastric cancer is a significant contributor to worldwide cancer deaths with limited treatment options and poor patient survival. MicroRNAs play crucial roles as potential oncogenic factors or tumor suppressors in cancers by modulating cell cycle progression, proliferation, migration, invasion, and apoptosis. However, the functional implications of miR-103a-3p in gastric cancer remain poorly known. The current study demonstrates a noteworthy increase in the expression of miR-103a-3p in gastric cancer tissues when compared to neighboring non-cancerous tissues. Our functional investigations indicate that the upregulation of miR-103a-3p contributes to enhanced proliferation, invasion, and migration capabilities in gastric cancer cells. After mechanistic studies, our findings indicate that miR-103a-3p may directly target insulin-like growth factor binding protein 5 (IGFBP5) in gastric cancer. Moreover, rescue experiments reveal that IGFBP5 overexpression can attenuate the progression induced by miR-103a-3p in gastric cancer cells. In summary, our findings suggest that the miR-103a-3p/IGFBP5 axis may play a role in gastric cancer progression, highlighting its potential as a therapeutic target and prognostic marker.