ArticleScientific reports2026
Identification of TMEM59L as a potential diagnosis, prognosis and immunotherapy biomarker for colon adenocarcinoma.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- TMEM59L promotes neuroendocrine differentiation and enzalutamide resistance in prostate cancer by regulating MUC1/β-catenin/MYC axis.Clinical and translational medicine · 2026Article
- Cancer-associated fibroblasts-derived exosomal circ_0067557 promotes colorectal cancer epithelial-mesenchymal transition via BHLHE40-mediated transcriptional activation of OTUB2.Biology direct · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Transmembrane protein 59-like (TMEM59L) has been implicated in malignant tumors; however, its role in colon adenocarcinoma (COAD) remains poorly understood. This study aimed to investigate the diagnostic and prognostic potential of TMEM59L in COAD, explore its association with the tumor microenvironment (TME) and potential implications for immunotherapy response. TMEM59L expression was analyzed in COAD tissue and serum samples using data from TCGA and GEO. Validation was conducted through immunohistochemistry (tissue) and ELISA (serum). Diagnostic performance was assessed using receiver operating characteristic (ROC) curve analysis; prognostic relevance was evaluated with Kaplan-Meier survival analysis, Cox regression, and nomograms. Functional enrichment analyses were performed to identify associated pathways. Immune cell infiltration was estimated using ssGSEA and single-cell data from TISCH. Immunotherapy response was predicted based on TIDE scores. In vitro, TMEM59L-overexpressing HCT116 cells were used to assess proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) using colony formation, Transwell, qPCR, and western blot assays. TMEM59L expression was significantly downregulated in COAD tissues but elevated in serum samples. High tissue expression was associated with advanced tumor stage and poorer overall survival. Genes co-expressed with TMEM59L were enriched in cancer-related and immune-regulatory pathways. Although TMEM59L expression correlated with increased immune infiltration and immune checkpoint gene expression, high levels predicted poorer response to immunotherapy. Cellular experiments demonstrated that TMEM59L overexpression enhanced proliferation, migration, invasion, and induced EMT (decreased E-cadherin; increased N-cadherin, VE-cadherin, and MMP14) in HCT116 cells. TMEM59L shows promise as a diagnostic and prognostic biomarker in COAD, with potential roles in modulating the TME, EMT, and immunotherapy response.
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.