ArticleCancer medicine2026
Stanniocalcin 2-Induced Autophagy Confers Resistance of Lung Cancer Cells to EGFR Inhibition via the ERK/Beclin 1 Signaling.
Article in Cancer medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Advances in understanding the mechanisms underlying acquired resistance to third-generation tyrosine kinase inhibitors in non-small cell lung cancer.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
7 authors.
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Abstract
backgroundAlthough epidermal growth factor receptor tyrosine kinase inhibitors (EGFR TKIs) are effective in treating NSCLC with EGFR mutations, the development of resistance limits their long-term efficacy. Autophagy has been implicated as a potential mechanism behind this acquired resistance. This study aims to investigate the role of Stanniocalcin 2 (STC2) in mediating autophagy and its contribution to EGFR TKI resistance.
methodsSTC2 expression was manipulated to examine its effects on autophagy and EGFR TKI resistance both in vitro and in vivo. Autophagic activity was assessed by measuring LC3B-II expression levels, the number of LC3 puncta, and the accumulation of autophagic vacuoles. Pharmacological inhibitors and small interfering RNA (siRNA) were used to assess whether the regulatory relationship between STC2 and Beclin 1 was involved in STC2-mediated autophagy and EGFR TKI resistance.
resultsHere, we found that STC2 was associated with increased autophagic activity, as evidenced by elevated LC3B-II levels, enhanced LC3 puncta formation, and increased accumulation of autophagic vacuoles. Conversely, STC2 knockdown resulted in reduced autophagic activity. We identified that STC2 is associated with ERK1/2 activation and Beclin 1-related autophagic activity. Importantly, inhibiting autophagy reversed the resistance to EGFR TKIs induced by STC2, as demonstrated in vitro and in vivo xenograft mouse models.
conclusionThese findings suggest that STC2 appears to promote cytoprotective autophagy, and targeting the STC2-associated ERK/Beclin 1 signaling axis may offer a promising strategy to overcome resistance to EGFR TKIs.
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