ArticleCancer research2012
Leptin mediates tumor-stromal interactions that promote the invasive growth of breast cancer cells.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.
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
65 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.
- Advances in the Prevention and Treatment of Obesity-Driven Effects in Breast Cancers.Frontiers in oncology · 2022Pooled it
- Targeting Obesity-Associated Breast Cancer: Curcumin Counteracts Leptin-Induced Tumorigenic and Metastatic Traits in MCF-7 and MDA-MB-231 Breast Cancer Cells.International journal of molecular sciences · 2026Article
- Adipocyte-derived estrogen signaling influences TROP2 expression in ERα-positive breast cancer.Frontiers in endocrinology · 2026Article
- Adipocyte‑derived extracellular vesicles sustain mitochondrial metabolism in breast cancer cells: New insights into the cross‑talk between cancer cells and the tumor microenvironment.International journal of oncology · 2025Article
- MIG6 loss confers resistance to ALK/ROS1 inhibitors in NSCLC through EGFR activation by low-dose EGF.JCI insight · 2023Article
- Role of Leptin and Adiponectin in Carcinogenesis.Cancers · 2023Review
- Leptin: A Heavyweight Player in Obesity-Related Cancers.Biomolecules · 2023Review
- Crosstalk of Inflammatory Cytokines within the Breast Tumor Microenvironment.International journal of molecular sciences · 2023Review
- Editorial: Adipokines and hormone-dependent cancers.Frontiers in endocrinology · 2023Article
- Effects of adipocyte-conditioned cell culture media on S1P treatment of human triple-negative breast cancer cells.PloS one · 2023Article
- Leptin stimulates migration and invasion and maintains cancer stem‑like properties in gastric cancer cells.Oncology reports · 2022Article
- Obesity and Breast Cancer Risk: The Oncogenic Implications of Metabolic Dysregulation.The Journal of clinical endocrinology and metabolism · 2022Article
- Targeting obesity-related dysfunction in hormonally driven cancers.British journal of cancer · 2021Review
- Article
- S100A4 Is Involved in Stimulatory Effects Elicited by the FGF2/FGFR1 Signaling Pathway in Triple-Negative Breast Cancer (TNBC) Cells.International journal of molecular sciences · 2021Article
- Tumor Metabolic Reprogramming by Adipokines as a Critical Driver of Obesity-Associated Cancer Progression.International journal of molecular sciences · 2021Review
- Targeting Metabolic Cross Talk Between Cancer Cells and Cancer-Associated Fibroblasts.Advances in experimental medicine and biology · 2021Article
- Article
- Article
- Stromal-associated cytokines bias the interplay between gene expression and DNA methylation in human breast cancers.Epigenetics · 2020Article
5 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
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Obesity confers risks to cancer development and progression but the mechanisms underlying these risks remain unclear. In this study, we identify a role for the obesity cytokine leptin, which has been implicated previously in breast cancer development, as a determinant for the tumor-promoting activity of cancer-associated fibroblasts (CAF) in both wild-type (WT) and K303R mutant estrogen receptor-α (ERα)-expressing breast cancer cells. Human CAFs stimulated a greater increase in the proliferation and migration of breast cancer cells expressing the K303R-ERα hyperactive receptor than WT-ERα-expressing cells. A concomitant increase was seen in leptin receptor isoform expression and activation of the leptin signaling pathway in cells expressing K303R-ERα compared with WT-ERα, correlating with leptin effects on cell growth, motility, and invasiveness in mutant cells. Epidermal growth factor and other factors secreted by K303R-ERα cells stimulated CAF proliferation, migration, and subsequent leptin secretion. Moreover, K303R-ERα expression generated a leptin hypersensitive phenotype in vivo. Together, our results reveal a bidirectional cross-talk between breast cancer cells and "educated" CAFs that drives tumor progression via leptin signaling. In elucidating a mechanism that connects obesity and cancer, these findings reinforce the concept that blocking cancer-stromal cell communication may represent an effective strategy for targeted therapy of breast cancer.
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.