ArticleInternational journal of cancer2014
Adrenomedullin is a therapeutic target in colorectal cancer.
Article in International journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 27 citations in OpenAlex.
- Adrenomedullin 2 drives intratumoral cancer cell invasion, intravasation and metastasis.Oncogene · 2026Article
- Multidimensional investigation of thyroid hormones and prostate cancer: insights from NHANES, Mendelian randomization, genetic markers, and bioinformatics analyses.Discover oncology · 2025Article
- Unraveling the role of GPCR signaling in metabolic reprogramming and immune microenvironment of lung adenocarcinoma: a multi-omics study with experimental validation.Frontiers in immunology · 2025Article
- Adrenomedullin induces cisplatin chemoresistance in ovarian cancer through reprogramming of glucose metabolism.Journal of translational internal medicine · 2023Article
- Peptidergic Systems and Cancer: Focus on Tachykinin and Calcitonin/Calcitonin Gene-Related Peptide Families.Cancers · 2023Review
- Gel-forming antagonist provides a lasting effect on CGRP-induced vasodilation.Frontiers in pharmacology · 2022Article
- Insight into the Web of Stress Responses Triggered at Gene Expression Level by Porphyrin-PDT in HT29 Human Colon Carcinoma Cells.Pharmaceutics · 2021Article
- Targeting Adrenomedullin in Oncology: A Feasible Strategy With Potential as Much More Than an Alternative Anti-Angiogenic Therapy.Frontiers in oncology · 2020Review
- Adrenomedullin inhibits tumor metastasis and is associated with good prognosis in triple-negative breast cancer patients.American journal of translational research · 2020Article
- Article
- Degranulation of mast cells induced by gastric cancer-derived adrenomedullin prompts gastric cancer progression.Cell death & disease · 2018Article
- Small molecules related to adrenomedullin reduce tumor burden in a mouse model of colitis-associated colon cancer.Scientific reports · 2017Article
- The role of adrenomedullin in the pathogenesis of gastric cancer.Oncotarget · 2017Article
- Down-regulation of malignant potential by alpha linolenic acid in human and mouse colon cancer cells.Familial cancer · 2015Article
- Adrenomedullin and tumour microenvironment.Journal of translational medicine · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 4 countries.
Funding
Abstract
The KRAS oncogene influences angiogenesis, metastasis and chemoresistance in colorectal cancers (CRCs), and these processes are all enhanced in hypoxic conditions. To define functional activities of mutant KRAS in a hypoxic microenvironment, we first performed cDNA microarray experiments in isogenic DKs5 and DKO3 colon cancer cell lines that differ only by their expression of mutant KRAS (K-ras(D13)). Adrenomedullin (ADM) was identified as one of the most significantly upregulated genes in DKs5 cells that express the KRAS oncogene in hypoxia (3.2-fold, p = 1.47 × 10(-5)). Ectopic expression of mutant KRAS (K-ras(V12)) in Caco-2 cells (K-ras(WT)) induced ADM, whereas selective knockdown of mutant KRAS alleles (K-ras(D13) or K-ras(V12)) in HCT116, DLD1 and SW480 colon cancer cells suppressed the expression of ADM in hypoxia. Knockdown of ADM in colon tumor xenografts blocked angiogenesis and stimulated apoptosis, resulting in tumor suppression. Furthermore, ADM also regulated colon cancer cell invasion in vitro. Among 56 patients with CRC, significantly higher expression levels of ADM were observed in samples harboring a KRAS mutation. Collectively, ADM is a new target of oncogenic KRAS in the setting of hypoxia. This observation suggests that therapeutic targets may differ depending upon the specific tumor microenvironment.
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.