ArticleNeoplasia (New York, N.Y.)2005
Persistent STAT3 activation in colon cancer is associated with enhanced cell proliferation and tumor growth.
Article in Neoplasia (New York, N.Y.), 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 219 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
219 citing papers in PubMed, 432 citations in OpenAlex.
- Enhanced antitumor efficacy of sulfasalazine and mesalazine in colorectal cancer through modulatory action of Lacticaseibacillus rhamnosus GG.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Preventive Effect of Helicobacter pylori Treatment on Colorectal Cancer Incidence and Mortality.Journal of gastroenterology and hepatology · 2026Article
- Beyond the Stomach: Exploring the Role ofExpert reviews in molecular medicine · 2026Review
- Uncovering molecular pathways in appendiceal cancer: A comprehensive characterization for precision oncology.American journal of surgery · 2026Article
- Targeting STAT3 by SH-4-54 suppresses the occurrence and inactivates oxidative phosphorylation in small-cell lung cancer via the SRC signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Advances in immunotherapy for colorectal cancer: overcoming resistance in mismatch repair-proficient tumors.Cancer cell international · 2026Review
- Splicing Factor 3a Subunit 1 Promotes Colorectal Cancer Growth via Anti-Apoptotic Effects of Syntaxin12.International journal of molecular sciences · 2026Article
- Article
- Targeting SHP-1 to alleviate testicular inflammation and apoptosis in a Poly(I:C)-induced orchitis model.European journal of medical research · 2025Article
- Silymarin induces multiple myeloma cell apoptosis by inhibiting the JAK2/STAT3 signaling pathway.Oncology letters · 2025Article
- Molecular mechanisms underlying TXNIP's anti-tumor role in breast cancer, including interaction with a novel, pro-tumor partner: CAST.Cell death & disease · 2025Article
- Targeting STAT3 with SH-4-54 suppresses stemness and chemoresistance in cancer stem-like cells derived from colorectal cancer.World journal of clinical oncology · 2025Article
- Long non-coding RNAs (lncRNAs) in cancer development: new insight from STAT3 signaling pathway to immune evasion.Clinical and experimental medicine · 2025Review
- Chronic stress synergizes withFrontiers in immunology · 2025Article
- The MicroRNA miR-223 Constrains Colitis-associated Tumorigenesis by Limiting Myeloid Cell Infiltration and Chemokine Expression.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Effect of Soy Isoflavone on Prostate Cancer Cell Apoptosis Through Inhibition of STAT3, ERK, and AKT.Current issues in molecular biology · 2024Article
- Bioengineered Anthocyanin-Enriched Tomatoes: A Novel Approach to Colorectal Cancer Prevention.Foods (Basel, Switzerland) · 2024Review
- SNORA28 Promotes Proliferation and Radioresistance in Colorectal Cancer Cells through the STAT3 Pathway by Increasing H3K9 Acetylation in the LIFR Promoter.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- From bench to bedside: the past, present and future of IL-21 immunotherapy.Medical oncology (Northwood, London, England) · 2024Review
159 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal carcinoma (CRC) is a major cause of morbidity and mortality in Western countries. It has so far been molecularly defined mainly by alterations of the Wnt pathway. We show here for the first time that aberrant activities of the signal transducer and activator of transcription STAT3 actively contribute to this malignancy and, thus, are a potential therapeutic target for CRC. Constitutive STAT3 activity was found to be abundant in dedifferentiated cancer cells and infiltrating lymphocytes of CRC samples, but not in non-neoplastic colon epithelium. Cell lines derived from malignant colorectal tumors lost persistent STAT3 activity in culture. However, implantation of colon carcinoma cells into nude mice resulted in restoration of STAT3 activity, suggesting a role of an extracellular stimulus within the tumor microenvironment as a trigger for STAT activation. STAT3 activity in CRC cells triggered through interleukin-6 or through a constitutively active STAT3 mutant promoted cancer cell multiplication, whereas STAT3 inhibition through a dominant-negative variant impaired IL-6-driven proliferation. Blockade of STAT3 activation in CRC-derived xenograft tumors slowed down their development, arguing for a contribution of STAT3 to colorectal tumor growth.
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.