ArticleInternational dental journal2026
Chemokine-Like Receptor 1 Knockdown Suppresses Oral Squamous Cell Carcinoma Progression by Reducing Oxidative Phosphorylation.
Article in International dental journal, 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOral squamous cell carcinoma (OSCC) is a common oral cavity malignancy with a poor prognosis. Although chemokine-like receptor 1 (CMKLR1) has been implicated in tumor progression in several types of cancer, its role and underlying mechanisms in OSCC remain unclear. In this study, we examined the role and mitochondrial metabolism pattern of CMKLR1 in OSCC progression.
methodsCMKLR1 expression was evaluated using data obtained from The Cancer Genome Atlas database and from immunohistochemical, RT-qPCR, and Western blotting analyses involving OSCC tissues and cell lines. Functional assays focusing on proliferation, migration, invasion, and colony formation were conducted after CMKLR1 knockdown or overexpression in OSCC cells. Proteomic analyses were conducted to identify CMKLR1-associated signaling pathways. Seahorse assays were used to assess mitochondrial oxidative phosphorylation (OXPHOS). In addition, the effect of mitochondrial inhibition with IACS-010759 was evaluated in CMKLR1-overexpressing models. Finally, signaling dependency was tested through PI3K/AKT inhibition and PGC-1α depletion.
resultsCMKLR1 expression was significantly elevated in OSCC, correlating with advanced OSCC, lymph node metastasis, and poor prognosis. CMKLR1 knockdown inhibited cell proliferation, migration, invasion, and epithelial-to-mesenchymal transition in vitro and suppressed tumor growth in vivo, whereas CMKLR1 overexpression had the opposite effect. Proteomic profiling and metabolic assays revealed that CMKLR1 knockdown suppressed mitochondrial function, decreased OXPHOS activity, and reduced ATP production. Additionally, pharmacological inhibition of OXPHOS with IACS-010759 significantly abrogated the tumor-promoting effects driven by CMKLR1 overexpression, thereby supporting a CMKLR1-OXPHOS regulatory axis in OSCC. Mechanistically, CMKLR1 activated PI3K/AKT signaling and induced PGC-1α production. Pharmacological blockade of PI3K/AKT abrogated CMKLR1-dependent PGC-1α upregulation, and PGC-1α depletion attenuated CMKLR1-driven mitochondrial respiration.
conclusionsCMKLR1 is a novel driver of OXPHOS in OSCC that functions through the PI3K/AKT/PGC-1α axis. Targeting mitochondrial metabolism may represent a promising therapeutic strategy for patients with overexpression of CMKLR1 and OSCC.
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.