ArticleOncogene2022
Downregulation of TEX11 promotes S-Phase progression and proliferation in colorectal cancer cells through the FOXO3a/COP1/c-Jun/p21 axis.
Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Exploring the prognostic value and biomarker of TEX11 in breast cancer via PANoptosis.Breast cancer (Tokyo, Japan) · 2026Article
- Gambogic acid suppresses osteosarcoma progression through upregulation of FOXO3a.Discover oncology · 2025Article
- Identification and validation of biomarkers related to centrosome replication in ulcerative colitis based on bulk transcriptome, single-cell RNA sequencing and experiments.Frontiers in immunology · 2025Article
- Tumor-secreted LCN2 impairs gastric cancer progression via autocrine inhibition of the 24p3R/JNK/c-Jun/SPARC axis.Cell death & disease · 2024Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) is the most common digestive tract malignancy, attributing to approximately 9.4% of global cancer-related deaths. However, the pathogenesis of CRC is poorly understood. The testis-expressed 11 (TEX11) gene is located on the X chromosome and is required for spermatogenesis, and is reported might serve as a biomarker for early onset CRC according to database analysis. However, the role played by TEX11 in cancer progression remains to be investigated. In this study, we show that TEX11 expression is significantly downregulated in CRC cell lines and clinical CRC tissue samples, and TEX11 expression correlates with poor prognosis in CRC patients. We further demonstrate that TEX11 can significantly inhibit the proliferative capacity of CRC cells in vitro and in vivo. Mechanistically, we demonstrate that TEX11 promotes transcription of COP1 by upregulating FOXO3a expression. This enhanced COP1 expression subsequently accelerates the degradation of the negative transcriptional regulator c-Jun, which, in turn, enhances p21 transcription inhibiting CRC cell cycle progression and proliferation. Overall, our findings suggest that TEX11 may be a valuable therapeutic target for the treatment of CRC.
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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.