ArticleAutophagy reports2022
SQSTM1/p62 as a therapeutic target in cancer.
Article in Autophagy reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- The Roles of SQSTM1/p62 in Selective Autophagy and Oncogenic Signaling.International journal of molecular sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell survival depends on dynamic interactions among the signaling pathways that control the endoplasmic reticulum (ER) stress response, macroautophagy/autophagy and apoptotic cell death. Our recent study reported an association of cytoplasmic SQSTM1/p62-mediated autophagy with disease progression and therapy resistance in head and neck squamous cell carcinoma (HNSCC). Synthetic small molecule ligands of SQSTM1 activate autophagic flux by binding the SQSTM1 ZZ domain and promoting self-oligomerization. Importantly, we found that the combination of pharmacological activation of SQSTM1 and therapeutic radiation promotes formation of ubiquitinated CASP8 (caspase 8) aggresomes that lead to apoptotic cell death of HNSCC. This finding suggests the potential for the development of a novel therapeutic strategy involving pharmacological activation of SQSTM1 in intrinsically apoptosis-resistant and therapy-resistant cancer cells.
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.