ArticleCell reports2022
AKTIP loss is enriched in ERα-positive breast cancer for tumorigenesis and confers endocrine resistance.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
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- Melatonin modulates SHH/GLI3 signaling and placental angiogenesis to counter acrylamide embryotoxicity.Journal of molecular histology · 2025Article
- STAT3: Key targets of growth-promoting receptor positive breast cancer.Cancer cell international · 2024Review
- Targeting metabolic sensing switch GPR84 on macrophages for cancer immunotherapy.Cancer immunology, immunotherapy : CII · 2024Article
- Transglutaminase 2 regulates endothelial cell calcification via IL-6-mediated autophagy.Frontiers in pharmacology · 2024Article
- Emerging roles of 3D-culture systems in tackling tumor drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2023Review
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
Recurrent deletion of 16q12.2 is observed in luminal breast cancer, yet the causal genomic alterations in this region are largely unknown. In this study, we identify that loss of AKTIP, which is located on 16q12.2, drives tumorigenesis of estrogen receptor alpha (ERα)-positive, but not ERα-negative, breast cancer cells and is associated with poor prognosis of patients with ERα-positive breast cancer. Intriguingly, AKTIP-depleted tumors have increased ERα protein level and activity. Cullin-associated and neddylation-dissociated protein 1 (CAND1), which regulates the cullin-RING E3 ubiquitin ligases, protects ERα from cullin 2-dependent proteasomal degradation. Apart from ERα signaling, AKTIP loss triggers JAK2-STAT3 activation, which provides an alternative survival signal when ERα is inhibited. AKTIP-depleted MCF7 cells and ERα-positive patient-derived organoids are more resistant to ERα antagonists. Importantly, the resistance can be overcome by co-inhibition of JAK2/STAT3. Together, our results highlight the subtype-specific functional consequences of AKTIP loss and provide a mechanistic explanation for the enriched AKTIP copy-number loss in ERα-positive breast cancer.
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