ReviewInternational journal of molecular sciences2018
The Multifaceted Role of STAT3 in Mammary Gland Involution and Breast Cancer.
Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.
- Abrupt involution induces inflammation, estrogenic signaling, and hyperplasia linking lack of breastfeeding with increased risk of breast cancer.Breast cancer research : BCR · 2019Pooled it
- STAT3 suppresses palmitic acid-induced apoptosis and fatty acid oxidation dysfunction in bovine mammary epithelial cells by transcriptionally activating CPT1A.Science China. Life sciences · 2026Article
- Postpartum breast cancer as a distinct oncologic entity: linking physiological tissue remodelling to tumor biology and clinical translation.Breast cancer research : BCR · 2026Review
- Out of Nucleus: Serine 727 Phosphorylation Orchestrates Non-Canonical STAT3 Functions-Relevance to Triple-Negative Breast Cancer.International journal of molecular sciences · 2026Review
- Little women: the relevance and reliance on mouse models for mammary gland research and next steps for translation.Journal of mammary gland biology and neoplasia · 2025Review
- Reproductive state controls transcription in the murine liver, with implications for breast cancer liver metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The Roles of STAT3 and STAT5 in Breast Cancer.Cancers · 2025Review
- From Embryogenesis to Senescence: The Role of Mammary Gland Physiology in Breast Cancer Risk.Cancers · 2025Review
- Machine learning-based integration of DCE-MRI radiomics for STAT3 expression prediction and survival stratification in breast cancer.Frontiers in immunology · 2025Article
- Relationship between breast tissue involution and breast cancer.Frontiers in oncology · 2025Review
- Mcam stabilizes a luminal progenitor-like breast cancer cell state via Ck2 control and Src/Akt/Stat3 attenuation.NPJ breast cancer · 2024Article
- Using Organoids to Tap Mammary Gland Diversity for Novel Insight.Journal of mammary gland biology and neoplasia · 2024Review
- Toward Characterizing Lymphatic Vasculature in the Mammary Gland During Normal Development and Tumor-Associated Remodeling.Journal of mammary gland biology and neoplasia · 2024Review
- Status of breast cancer detection in young women and potential of liquid biopsy.Frontiers in oncology · 2024Review
- Targeting STAT3 Enzyme for Cancer Treatment.Mini reviews in medicinal chemistry · 2024Review
- PCBP1 regulates LIFR through FAM3C to maintain breast cancer stem cell self-renewal and invasiveness.Cancer biology & therapy · 2023Article
- Kindlin-2 in myoepithelium controls luminal progenitor commitment to alveoli in mouse mammary gland.Cell death & disease · 2023Article
- Fur removal promotes an earlier expression of involution-related genes in mammary gland of lactating mice.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2023Article
- Effects of sustained hyperprolactinemia in late gestation on the mammary parenchymal tissue transcriptome of gilts.BMC genomics · 2023Article
- Tristetraprolin promotes survival of mammary progenitor cells by restraining TNFα levels.Frontiers in cell and developmental biology · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Since seminal descriptions of signal transducer and activator of transcription 3 (STAT3) as a signal transducer and transcriptional regulator, which is most usually activated by phosphorylation of a specific tyrosine residue, a staggering wealth of research has delineated the key role of this transcription factor as a mediator of mammary gland postlactational regression (involution), and paradoxically, a pro-survival factor in breast cancer and some breast cancer cell lines. STAT3 is a critical regulator of lysosomal-mediated programmed cell death (LM-PCD) during mammary gland involution, where uptake of milk fat globules, and consequent high levels of free fatty acids, cause permeabilisation of lysosomal vesicle membranes, in turn leading to cathepsin protease leakage and cell death. A recent proteomic screen of STAT3-induced changes in lysosomal membrane protein components has highlighted wide-ranging effects of STAT3, which may coordinate LM-PCD via the stimulation of endocytosis, intracellular trafficking, and lysosome biogenesis. In parallel, STAT3 regulates the acute phase response during the first phase of involution, and it contributes to shaping the pro-tumourigenic 'wound healing' signature of the gland during the second phase of this process. STAT3 activation during involution is important across species, although some differences exist in the progression of involution in dairy cows. In breast cancer, a number of upstream regulators can lead to STAT3 activation and the effects of phosphorylation of STAT3 are equally wide-ranging. Recent studies have implicated microRNAs in some regulatory pathways. In this review, we will examine the multifaceted role of STAT3 in mammary gland involution and tumourigenesis, incorporating a review of these fundamental processes in tandem with a discussion of recent developments in this field.
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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.