ArticleInternational journal of oncology2025
RHOT1‑mediated molecular mechanism of mitochondrial dysfunction and its phenotypic effects on gastric cancer cells.
Article in International journal of oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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
4 citing papers in PubMed.
- Arbutin as a promising cardioprotective anticancer adjuvant with doxorubicin in solid Ehrlich carcinoma through targeting NEK7-dependent inflammasome/SIRT1/caspase-3/oxidative stress pathways.Molecular and cellular biochemistry · 2026Article
- Cross-species transcriptomic integration reveals a MIRO1-mediated macrophage-T cell axis in glioma.Life science alliance · 2026Article
- Mitophagy interacts with mitochondrial dynamics and biogenesis, acting as a double-edged sword in digestive cancer.iScience · 2026Review
- SIRT1 as a masterful reciprocal regulator of molecular mechanisms and signaling pathways involved in tumor growth and expansion.Clinical and experimental medicine · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitophagy, a selective autophagy process that targets damaged mitochondria, plays a critical role in cellular homeostasis and disease progression, including tumorigenesis. Ras homolog family member T1 (RHOT1), a mitochondria‑associated protein, has been reported to regulate mitochondrial dynamics and energy metabolism. However, its role in gastric cancer (GC) remains unclear. The present study aimed to investigate the function of RHOT1 in GC progression and its mechanistic link with mitochondrial quality control. To achieve this, RHOT1 was silenced in GC cells and its effect on the PINK1/Parkin pathway, mitochondrial homeostasis and cellular behavior examined. The study employed qPCR and western blotting to evaluate gene and protein expression, siRNA transfection to silence RHOT1 and flow cytometry, CCK‑8 proliferation, wound‑healing, and Transwell assays to investigate mitochondrial function and cellular phenotypes. Silencing RHOT1 reduced
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.