ArticleThe Journal of clinical investigation2015
LKB1 loss promotes endometrial cancer progression via CCL2-dependent macrophage recruitment.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
62 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.
- Pooled it
- Molecular insights and therapeutic implications for the tumor suppressor role of LKB1 in non-small cell lung cancer.Cancer letters · 2026Review
- FBXW7 Inhibited M2 Macrophage Polarization in Endometrial Cancer by Reducing CCL2 Secretion Through Ubiquitination of MYBL2 Subtitle: The Role of FBXW7 on M2 Macrophage Polarization in EC.Biochemical genetics · 2026Article
- TAMs in the Gynecological Tumor Microenvironment: Insights from Cross-Cancer Studies for Immunotherapy.Cancers · 2026Review
- The role of extracellular vesicles in the communication between endometrial cancer cells and tumour-associated macrophages: a review.Journal of cancer research and clinical oncology · 2025Review
- Suppression of STK11 induces expansion of polymorphonuclear myeloid-derived suppressive cells and activation of immune signaling in breast cancer.Cancer immunology, immunotherapy : CII · 2025Article
- Antagonism of estrogen-related receptor-α inhibits mitochondrial oxidative phosphorylation and reduces M2 macrophage infiltration in endometrial cancer.Journal for immunotherapy of cancer · 2025Article
- Targeting LKB1/STK11-mutant cancer: distinct metabolism, microenvironment, and therapeutic resistance.Trends in pharmacological sciences · 2025Review
- Association of peripheral monocytic myeloid-derived suppressor cells with molecular subtypes in single-center endometrial cancer patients receiving carboplatin + paclitaxel/avelumab (MITO-END3 trial).Cancer immunology, immunotherapy : CII · 2025Article
- Focusing on the interplay between tumor-associated macrophages and tumor microenvironment: from mechanism to intervention.Theranostics · 2025Review
- Epidemiology, molecular typing, microbiome-immune interactions and treatment strategies of endometrial cancer: a review.Frontiers in immunology · 2025Review
- Relevance of mutation-derived neoantigens and non-classical antigens for anticancer therapies.Human vaccines & immunotherapeutics · 2024Review
- Article
- Identification of key genes associated with endometriosis and endometrial cancer by bioinformatics analysis.Frontiers in oncology · 2024Article
- Immune cell networking in solid tumors: focus on macrophages and neutrophils.Frontiers in immunology · 2024Review
- Predictive value of CCL2 in the prognosis and immunotherapy response of glioblastoma multiforme.BMC genomics · 2023Article
- Article
- FAM171B stabilizes vimentin and enhances CCL2-mediated TAM infiltration to promote bladder cancer progression.Journal of experimental & clinical cancer research : CR · 2023Article
- Multi-omics characteristics of tumor-associated macrophages in the tumor microenvironment of gastric cancer and their exploration of immunotherapy potential.Scientific reports · 2023Article
- Review
2 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
13 authors at 4 institutions in 1 country.
Funding
Abstract
Endometrial cancer is the most common gynecologic malignancy and the fourth most common malignancy in women. For most patients in whom the disease is confined to the uterus, treatment results in successful remission; however, there are no curative treatments for tumors that have progressed beyond the uterus. The serine/threonine kinase LKB1 has been identified as a potent suppressor of uterine cancer, but the biological modes of action of LKB1 in this context remain incompletely understood. Here, we have shown that LKB1 suppresses tumor progression by altering gene expression in the tumor microenvironment. We determined that LKB1 inactivation results in abnormal, cell-autonomous production of the inflammatory cytokine chemokine (C-C motif) ligand 2 (CCL2) within tumors, which leads to increased recruitment of macrophages with prominent tumor-promoting activities. Inactivation of Ccl2 in an Lkb1-driven mouse model of endometrial cancer slowed tumor progression and increased survival. In human primary endometrial cancers, loss of LKB1 protein was strongly associated with increased CCL2 expression by tumor cells as well as increased macrophage density in the tumor microenvironment. These data demonstrate that CCL2 is a potent effector of LKB1 loss in endometrial cancer, creating potential avenues for therapeutic opportunities.
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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 OpenQuestion graph.