Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA325477 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Targeting metastasis stem cells through the fatty acid receptor CD36 (I)
| PRJNA296106 | ENA
Project description:Targeting metastasis stem cells through the fatty acid receptor CD36 (II)
| PRJNA296105 | ENA
Project description:Targeting metastasis stem cells through the fatty acid receptor CD36 (DID+, DID- and CD44DIM).
| PRJNA325647 | ENA
Project description:Targeting metastasis stem cells through the fatty acid receptor CD36
| PRJNA295964 | ENA
Project description:Breast tumors develop in a complex microenvironment whose main component is adipose tissue and gain aggressiveness through increased fatty acid uptake. Here, we demonstrated that palmitic acid (PA) induced ferroptosis in triple negative breast cancers (TNBC). We found that PA increases the protein expression levels of the long-chain fatty acid transporter CD36 leading to increased lipid uptake. Mechanistically, overexpression of CD36 increases lipid peroxidation, mitochondrial ROS production, the labile iron pool and especially Fe2+ content. Additionally, we found increased expression of ferroptotic target genes (HMOX1, ACSL1, SAT1) and decreased of anti-ferroptotic genes (GPX4 and FSP1) in TNBC following PA exposure. Overexpression of CD36 did not induce ferroptosis in estrogen receptor positive breast cancer. Clinically, higher CD36 expression correlated with the luminal androgen receptor (LAR) subtype of TNBC, known to exhibit a higher sensitivity to ferroptosis. Altogether, these data provide evidence for an essential role of the CD36 protein in the ferroptotic process induced by the saturated fatty acid PA, opening potential new therapeutic approaches promoting ferroptosis in the most aggressive breast cancers.
2025-10-10 | GSE306759 | GEO
Project description:Metastasis is the leading cause of cancer-related deaths. For most human cancers, the identity of the cells that initiate and promote metastasis is still unknown, hampering our ability to develop therapies to prevent or inhibit the spread of tumour cells to distant sites. Using an orthotopic model of human oral squamous cell carcinoma (OSCC), we have now identified a subpopulation of CD44bright cells within the primary lesion with the highest potential to develop lymph node and lung metastasis. This population is slow-cycling, expresses high levels of the receptor CD36 at the cell membrane and relies on fatty acid metabolism to thrive in lymph nodes and bronchoalveolar environments. Importantly, inhibition of CD36 by either shRNA or neutralizing monoclonal antibodies severely impairs metastatic spread of primary OSCC patient samples and established cell lines. Further underscoring its importance, CD36 overexpression in poorly disseminating tumours confers an aggressive metastatic behaviour. Analyses of public gene expression data indicate that the presence of the signature-defining CD36+ cells also strongly correlates with a poor prognosis in patients with lung SCC, ovarian cancer, bladder cancer, or luminal breast cancer. By identifying metastasis-promoting cells and then targeting them with CD36 inhibition, novel anti-metastatic therapies could be developed for patients with these types of tumours.
2016-12-16 | GSE72938 | GEO
Project description:Metastasis is the leading cause of cancer-related deaths. For most human cancers, the identity of the cells that initiate and promote metastasis is still unknown, hampering our ability to develop therapies to prevent or inhibit the spread of tumour cells to distant sites. Using an orthotopic model of human oral squamous cell carcinoma (OSCC), we have now identified a subpopulation of CD44bright cells within the primary lesion with the highest potential to develop lymph node and lung metastasis. This population is slow-cycling, expresses high levels of the receptor CD36 at the cell membrane and relies on fatty acid metabolism to thrive in lymph nodes and bronchoalveolar environments. Importantly, inhibition of CD36 by either shRNA or neutralizing monoclonal antibodies severely impairs metastatic spread of primary OSCC patient samples and established cell lines. Further underscoring its importance, CD36 overexpression in poorly disseminating tumours confers an aggressive metastatic behavior. Analyses of public gene expression data indicate that the presence of the signature-defining CD36+ cells also strongly correlates with a poor prognosis in patients with lung SCC, ovarian cancer, bladder cancer, or luminal breast cancer. By identifying metastasis-promoting cells and then targeting them with CD36 inhibition, novel anti-metastatic therapies could be developed for patients with these types of tumours.
2016-12-16 | GSE72935 | GEO
Project description:Metastasis is the leading cause of cancer-related deaths. For most human cancers, the identity of the cells that initiate and promote metastasis is still unknown, hampering our ability to develop therapies to prevent or inhibit the spread of tumour cells to distant sites. Using an orthotopic model of human oral squamous cell carcinoma (OSCC), we have now identified a subpopulation of CD44bright cells within the primary lesion with the highest potential to develop lymph node and lung metastasis. This population is slow-cycling, expresses high levels of the receptor CD36 at the cell membrane and relies on fatty acid metabolism to thrive in lymph nodes and bronchoalveolar environments. Importantly, inhibition of CD36 by either shRNA or neutralizing monoclonal antibodies severely impairs metastatic spread of primary OSCC patient samples and established cell lines. Further underscoring its importance, CD36 overexpression in poorly disseminating tumours confers an aggressive metastatic behaviour. Analyses of public gene expression data indicate that the presence of the signature-defining CD36+ cells also strongly correlates with a poor prognosis in patients with lung SCC, ovarian cancer, bladder cancer, or luminal breast cancer. By identifying metastasis-promoting cells and then targeting them with CD36 inhibition, novel anti-metastatic therapies could be developed for patients with these types of tumours.
2016-12-16 | GSE83346 | GEO
Project description:Metastasis is the leading cause of cancer-related deaths. For most human cancers, the identity of the cells that initiate and promote metastasis is still unknown, hampering our ability to develop therapies to prevent or inhibit the spread of tumour cells to distant sites. Using an orthotopic model of human oral squamous cell carcinoma (OSCC), we have now identified a subpopulation of CD44bright cells within the primary lesion with the highest potential to develop lymph node and lung metastasis. This population is slow-cycling, expresses high levels of the receptor CD36 at the cell membrane and relies on fatty acid metabolism to thrive in lymph nodes and bronchoalveolar environments. Importantly, inhibition of CD36 by either shRNA or neutralizing monoclonal antibodies severely impairs metastatic spread of primary OSCC patient samples and established cell lines. Further underscoring its importance, CD36 overexpression in poorly disseminating tumours confers an aggressive metastatic behaviour. Analyses of public gene expression data indicate that the presence of the signature-defining CD36+ cells also strongly correlates with a poor prognosis in patients with lung SCC, ovarian cancer, bladder cancer, or luminal breast cancer. By identifying metastasis-promoting cells and then targeting them with CD36 inhibition, novel anti-metastatic therapies could be developed for patients with these types of tumours.
2016-12-16 | GSE83276 | GEO
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO