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2000
Volume 21, Issue 4
  • ISSN: 1573-4099
  • E-ISSN: 1875-6697

Abstract

Background

Astragaloside IV (AS-IV) has been shown to have a curative effect on non-small cell lung cancer (NSCLC). This study aimed to elucidate the role of AS-IV in NSCLC cell anlotinib resistance (AR).

Methods

The NSCLC/AR cells, resistant to anlotinib, have been produced. The role of AS-IV in the AR of NSCLC cells about the miR-181a-3p/unfolded protein response (UPR)-endoplasmic reticulum associated degradation (ERAD) pathway was then discussed by treating the cells with anlotinib or AS-IV, or by manipulating them with inhibitors or mimics of miR-181a-3p, HRD1 or Derlin-1 overexpression plasmids.

Results

We found that AS-IV could suppress the AR of NSCLC cells. In addition, miR-181a-3p was elevated in NSCLC/AR cells. Functionally, AS-IV limited the AR of NSCLC cells by reducing miR-181a-3p. Further, activation of the UPR-ERAD pathway was correlated with AR in NSCLC cells. Increased sensitivity of NSCLC cells to anlotinib caused by miR-181a-3p inhibitor could be reversed by overexpression of HRD1 or Derlin-1.

Conclusion

This research revealed a promising NSCLC/AR treatment approach by showing that AS-IV exposed NSCLC cells to anlotinib by inhibiting the miR-181a-3p/UPR-ERAD axis.

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2024-01-17
2025-09-04
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  • Article Type:
    Research Article
Keyword(s): anlotinib; Astragaloside IV; ERAD; miR-181a-3p; non-small cell lung cancer; UPR
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