ArticleAmerican journal of cancer research2025
NUCKS1 exacerbates hepatocellular carcinoma cell proliferation and metastasis via the upregulation of Cdc42.
Article in American journal of cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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
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
Nuclear casein kinase and cyclin-dependent kinases substrate 1 (NUCKS1) is overexpressed in hepatocellular carcinoma (HCC), but its role and regulatory mechanism in the development and progression of HCC remains unknown. Here, we report that the RNA and protein levels of NUCKS1 were significantly increased in HCC tissues. The inhibition of NUCKS1 notably decreased the proliferation and migration of SNU449 and HepG2 cells. However, NUCKS1 overexpression exacerbated cell growth and migration. Additionally, NUCKS1 depletion reduced the sphere formation efficiency and inhibited tumorigenesis in vivo. Mechanistically, depletion of NUCKS1 downregulated the expression of cell division control protein 42 (Cdc42), and NUCKS1 directly bound to the promoter of Cdc42 and transcriptionally upregulated Cdc42, which promoted the development and progression of HCC. Furthermore, the expression of NUCKS1 was positively associated with Cdc42 in HCC tissues. Collectively, our data indicate that the increasing expression of NUCKS1 plays an oncogenic role and promotes progression via transactivation of Cdc42 expression in HCC.
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.