ArticleAnti-cancer drugs2026
The novel integrin-linked kinase inhibitor nilotinib suppresses cancer progression by promoting ubiquitylation of autoimmune regulator in oesophageal squamous cell carcinoma.
Article in Anti-cancer drugs, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Integrin-linked kinase (ILK) is a key oncogenic driver in oesophageal squamous cell carcinoma (ESCC). This study evaluated the antitumour effects of the novel ILK inhibitor Nilotinib and explored its downstream mechanisms. In vitro , TE-1 and KYSE150 cells were assessed using Cell Counting Kit-8, lactate dehydrogenase release, colony formation, 5-ehynyl-2 ' -deoxyuridine incorporation, flow cytometry, Transwell assays, and Western blotting to confirm ILK targeting and determine functional changes. Electron microscopy and fluorescent probes with flow cytometry were used to analyse mitochondrial alterations. In vivo , a nude mouse subcutaneous xenograft model was established to examine tumour growth after peritumoural Nilotinib administration; hematoxylin and eosin staining assessed tissue changes, and immunohistochemistry measured Ki67 and cleaved-caspase 3 expression. ILK overexpression alleviated Nilotinib-induced cytotoxicity, restored proliferation, increased proliferating cell nuclear antigen (PCNA) and Ki67, and reduced cleaved-caspase 3 and cleaved poly(ADP-ribose) polymerase (PARP), supporting ILK as a primary target. Nilotinib dose-dependently inhibited proliferation, invasion, and metastasis while promoting apoptosis, accompanied by downregulation of PCNA, Ki67, [matrix metalloproteinase 2 (MMP2), MMP9, and COX2] and upregulation of cleaved-caspase 3 and cleaved-PARP. In xenografts, Nilotinib significantly reduced tumour size and weight, decreased Ki67, and increased cleaved-caspase 3.RNA sequencing identified autoimmune regulator (AIRE) as a markedly downregulated molecule following Nilotinib treatment. Cycloheximide chase assays indicated accelerated AIRE protein degradation, while MG132 partially rescued AIRE levels, implicating proteasome-dependent degradation. Overall, Nilotinib suppresses ESCC progression by inhibiting ILK and destabilising AIRE, suggesting its potential as a targeted therapy for ILK-positive ESCC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.