ArticleOncology research2026
Cholecystokinin A Receptor Knockdown Diminishes Colon Cancer Cell Invasive Potential via Modulation of Integrin/FAK, EMT, and uPA/uPAR/MMP2 Axis.
Article in Oncology research, 2026. 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
Objectives: Cholecystokinin A receptor (CCKAR) has been linked to poor prognosis in colon cancer patients, but the role of CCKAR in colon cancer cell invasiveness and the underlying mechanisms remain elusive. This study aimed to explore the effect of CCKAR on the invasive potential of colon cancer cells. Methods: Different human colon cancer cell lines were used. Gene expression was evaluated by reverse transcription polymerase chain reaction (RT-PCR) and quantitative real-time RT-PCR (qPCR), while protein expression and phosphorylation were assessed by Western blotting. Cell motility and invasiveness were examined through wound healing and invasion assays, respectively. Results: Our results showed that CCKAR expression levels varied across colon cancer cell lines, with DLD-1 and LoVo cells showing high expression. Knockdown of CCKAR significantly impaired the cell motility and invasiveness of DLD-1 and LoVo cells, downregulated integrin β3 expression, and diminished the phosphorylation levels of focal adhesion kinase (FAK), Src, and paxillin. In addition, CCKAR knockdown modulated epithelial-mesenchymal transition (EMT) markers ZO-1, E-cadherin, and vimentin and reduced urokinase-type plasminogen activator (uPA), uPA receptor (uPAR), Rho GTPase cell division control protein 42 (CDC42) and RhoA, and matrix metalloproteinase-2 (MMP-2). Conclusions: These findings indicate that CCKAR knockdown impairs the invasiveness of colon cancer cells, which may be attributed to modulating integrin/FAK/Rho GTPases, EMT markers, and the uPA/uPAR axis. It suggests that targeting CCKAR may represent a potential therapeutic strategy for colon cancer treatment.
Indexed as
Identifiers
What 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.