ArticleBMC cancer2026
Regulation of natural killer cell infiltration and tumor progression by CMTM6 in gastric cancer.
Article in BMC cancer, 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
10 authors.
Funding
Abstract
backgroundTumor CMTM6 is known to regulate programmed death-ligand 1 expression and affect the cytotoxicity of infiltrating T cells, while its impact on natural killer (NK) cells and tumor malignancy remains to be fully understood. This study aimed to investigate the influences of tumor CMTM6 on NK cell infiltration and tumor progression.
methodsWe established animal models of gastric cancer to assess the effects of CMTM6 knockdown on the NK cell infiltration into the tumor. Tumor tissue microarray was used to evaluate the correlation between CMTM6 expression and tumor differentiation. Proteomic analysis was performed to identify potential downstream effectors of CMTM6, validated by coimmunoprecipitation. The lysosomal and proteasomal degradation of the effector was determined by cycloheximide chase given CMTM6 knockdown or over-expression in vitro.
resultsCMTM6 knockdown significantly enhanced the infiltration of NK cells into gastric tumors and suppressed tumor growth. CMTM6 protein level decreased in poorly differentiated gastric cancer, correlating with the loss of epithelial integrity. We identified poliovirus receptor-related 2 (PVRL2/Nectin-2) as a potential effector of CMTM6, which functions as an adhesion molecule critical for cellular junctions and the epithelial barrier. CMTM6 interacts with Nectin-2 via RAB14/RAB11 mediated trafficking, and CMTM6 inhibits Nectin-2 degradation through both lysosomal and proteasomal pathways.
conclusionsInhibition of CMTM6 expression enhances host anti-tumor immunity by increasing NK cell infiltration while potentially influencing the tumor progression.
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.