ArticlePloS one2016
Sam68 Mediates the Activation of Insulin and Leptin Signalling in Breast Cancer Cells.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- RNA-Binding Proteins in Adipose Biology: From Mechanistic Understanding to Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Role of Sam68 in different types of cancer (Review).International journal of molecular medicine · 2025Review
- The Expression of Genes Related to Reverse Cholesterol Transport and Leptin Receptor Pathways in Peripheral Blood Mononuclear Cells Are Decreased in Morbid Obesity and Related to Liver Function.International journal of molecular sciences · 2024Article
- Role of Sam68 as an adaptor protein in inflammatory signaling.Cellular and molecular life sciences : CMLS · 2024Review
- Validating Sam68 expression and protein level in breast cancer.Journal of medicine and life · 2023Article
- Decreased Expression of Sam68 Is Associated with Insulin Resistance in Granulosa Cells from PCOS Patients.Cells · 2022Article
- Research progress on RNA-binding proteins in breast cancer.Frontiers in oncology · 2022Review
- Sam68 contributes to intestinal inflammation in experimental and human colitis.Cellular and molecular life sciences : CMLS · 2021Article
- Article
- Role of Leptin in Inflammation and Vice Versa.International journal of molecular sciences · 2020Review
- Sam68 mediates leptin signaling and action in human granulosa cells: possible role in leptin resistance in PCOS.Endocrine connections · 2020Article
- Leptin, Adiponectin, and Sam68 in Bone Metastasis from Breast Cancer.International journal of molecular sciences · 2020Review
- SAM68 interaction with U1A modulates U1 snRNP recruitment and regulates mTor pre-mRNA splicing.Nucleic acids research · 2019Article
- Obesity and Breast Cancer: Role of Leptin.Frontiers in oncology · 2019Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity is a well-known risk factor for breast cancer development in postmenopausal women. High insulin and leptin levels seem to have a role modulating the growth of these tumours. Sam68 is an RNA-binding protein with signalling functions that has been found to be overexpressed in breast cancer. Moreover, Sam68 may be recruited to insulin and leptin signalling pathways, mediating its effects on survival, growth and proliferation in different cellular types. We aimed to study the expression of Sam68 and its phosphorylation level upon insulin and leptin stimulation, and the role of Sam68 in the proliferative effect and signalling pathways that are activated by insulin or leptin in human breast adenocarcinoma cells. In the human breast adenocarcinoma cell lines MCF7, MDA-MB-231 and BT-474, Sam68 protein quantity and gene expression were increased upon leptin or insulin stimulation, as it was checked by qPCR and immunoblot. Moreover, both insulin and leptin stimulation promoted an increase in Sam68 tyrosine phosphorylation and negatively regulated its RNA binding capacity. siRNA was used to downregulate Sam68 expression, which resulted in lower proliferative effects of both insulin and leptin, as well as a lower activation of MAPK and PI3K pathways promoted by both hormones. These effects may be partly explained by the decrease in IRS-1 expression by down-regulation of Sam68. These results suggest the participation of Sam68 in both leptin and insulin receptor signaling in human breast cancer cells, mediating the trophic effects of these hormones in proliferation and cellular growth.
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