ArticleJournal of bioenergetics and biomembranes2026
SPC25 promotes gastric cancer cells G1/S cell cycle transition and tumorigenesis by enhancing SLC1A5-mediated glutamine metabolism.
Article in Journal of bioenergetics and biomembranes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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
- Erratum issued
Authors and funding
4 authors.
Funding
Abstract
Although spindle pole body component 25 (SPC25) has been implicated in various cancers, its precise role in GC remains unexplored. This study aimed to investigate the role and mechanism of SPC25 in GC progression. SPC25 expression was analyzed using TCGA database and 40 paired GC clinical specimens. RT-qPCR, Western blot and immunohistochemistry (IHC) staining were performed to detect the expression of SPC25 in GC samples. Flow cytometry was conducted to assess the cell cycle, and commercial kits were used to measure the levels of glutamine, glutamic acid, α-Ketoglutaric acid (α-KG) and NADPH/NADP+. MeRIP-PCR was employed to explore the regulatory role of SPC25 on the m6A levels of SLC1A5. RNA immunoprecipitation (RIP) assay to test the binding between IGF2BP2 and SPC25 transcripts. Xenograft mouse model was constructed to assess the effect of SPC25 on tumor growth in vivo. SPC25 was significantly overexpressed in GC tissues and cell lines. Silencing SPC25 repressed G1/S cell cycle transition and downregulated the expressions of several key mitotic regulators. Moreover, the interference of SPC25 repressed glutamine metabolism in GC cells, as demonstrated by reduced glutamine consumption and decreased production of α-KG, glutamate and NADPH/NADP+. SPC25 overexpression exerted the opposite effects. Mechanistically, SPC25 promoted glutamine metabolism and cell cycle progression in GC by stabilizing SLC1A5 expression through IGF2BP2-mediated m6A modification. Animal study revealed that SPC25 knockdown suppressed tumor growth in vivo. SPC25, stabilizing SLC1A5 expression through IGF2BP2 mediated m6A modification, regulated glutamine metabolism, promoted gastric cancer cells G1/S cell cycle transition and drove tumor progression.
Indexed as
Identifiers
42012696What Socratic 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 Socratic graph.