ArticleDiscover oncology2025
SNX7 mediates inhibition of autophagy in prostate cancer via activation of CFLIP expression.
Article in Discover oncology, 2025. 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.
- Pan-cancer analysis of role of LOXL4 and experiment validation in osteosarcoma.Discover oncology · 2025Article
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
No grant is acknowledged in the PubMed record.
Abstract
backgroundProstate cancer (PC) is a major health concern among men worldwide, yet its underlying molecular mechanisms remain incompletely understood. Identifying key regulatory genes and signaling pathways involved in PC progression is essential for improving diagnosis and developing targeted therapies.
methodsProstate adenocarcinoma (PRAD) samples from The Cancer Genome Atlas (TCGA) and the GSE46602 dataset were analyzed using bioinformatics techniques in order to determine the hub gene linked to PC. Through cell experiments, we studied the effects of SNX7 and its related genes on PC cell proliferation, migration, invasion, and autophagy-related protein binding. Additionally, we looked into the connection between SNX7 expression and other immune cells.
resultsWe discovered that a favorable prognosis for patients with PC was linked to increased expression of SNX7. The function of SNX7 as a tumor suppressor gene in PC was further demonstrated by in vitro experiments, and its overexpression may successfully stop PC cell proliferation. CFLIP was positively correlated with SNX7, and its overexpression significantly reduced PC cell viability, migration, and invasion. Rescue experiments showed that SNX7 overexpression reversed the proliferative and invasive effects induced by CFLIP knockdown. Additionally, CFLIP knockdown enhanced the interaction between ATG3 and LC3A, whereas overexpression of SNX7 or CFLIP weakened this binding. SNX7 was also found to be associated with various immune cells, hinting at a prospective immunomodulatory role in PC.
conclusionThe research results showed that SNX7 activates the expression of CFLIP, inhibited the binding of ATG3 and LC3, and inhibited the occurrence of autophagy, emphasizing the potential diagnostic value of SNX7 in PC.
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.