ArticleiScience2022
MCM7 supports the stemness of bladder cancer stem-like cells by enhancing autophagic flux.
Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- The role of autophagy in periodontal diseases: a bibliometric analysis from 2006 to 2023.Frontiers in medicine · 2025Pooled it
- Multi-omics integration reveals that pyrimidine metabolism in lung adenocarcinoma drives an immunosuppressive microenvironment.iScience · 2026Article
- Mitophagy in bladder cancer: a double-edged sword in tumor progression and therapy.Journal of translational medicine · 2026Review
- Article
- DARS2 Promotes Bladder Cancer Progression by Enhancing PINK1-Mediated Mitophagy.International journal of biological sciences · 2025Article
- CCDC34 maintains stemness phenotype through β-catenin-mediated autophagy and promotes EGFR-TKI resistance in lung adenocarcinoma.Cancer gene therapy · 2025Article
- The splicing factor WBP11 mediates MCM7 intron retention to promote the malignant progression of ovarian cancer.Oncogene · 2024Article
- Review
- LIMP-2 enhances cancer stem-like cell properties by promoting autophagy-induced GSK3β degradation in head and neck squamous cell carcinoma.International journal of oral science · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy plays critical roles in the pluripotent stemness of cancer stem cells (CSCs). However, how CSCs maintain the elevated autophagy to support stemness remains elusive. Here, we demonstrate that bladder cancer stem-like cells (BCSLCs) are at slow-cycling state with enhanced autophagy and mitophagy. In these slow-cycling BCSLCs, the DNA replication initiator MCM7 is required for autophagy and stemness. MCM7 knockdown inhibits autophagic flux and reduces the stemness of BCSLCs. MCM7 can facilitate autolysosome formation through binding with dynein to promote autophagic flux. The enhanced autophagy/mitophagy helps BCSLCs to maintain mitochondrial respiration, thus inhibiting AMPK activation. AMPK activation can trigger switch from autophagy to apoptosis, through increasing BCL2/BECLIN1 interaction and inducing P53 accumulation. In summary, we find that MCM7 can promote autophagic flux to support.
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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.