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Triple Negative Breast Cancer (TNBC)

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Moderate Exercise Modulates Tumor Metabolism of Triple-Negative Breast Cancer

https://repositorio.usp.br/directbitstream/527c07c6-11cd-4ebf-a2c3-1ced8c0a0152/002999972.pdf


   
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Rapid Extensive Recurrence of Triple Negative Breast Cancer: Are Both Therapy and Cancer Biology the Culprit?

https://www.jocmr.org/index.php/JOCMR/article/view/2365/1375


   
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Combination of Ashwagandha Water Extract and Intermittent Fasting as a Therapy to Overcome Cisplatin Resistance in Breast Cancer: An in vitro and in vivo Study

"Antitumor Effect of WS Root Extract, Intermittent Fasting, Cisplatin, and Their Combinations

Based on the results of the in vitro assay, WSR extract was selected in addition to IF, cisplatin, and their combinations for further evaluation to assess the antitumor activity in Balb/C female mice. According to the results in Table 3, the treated groups showed a significant reduction (p < 0.05) in tumor size compared with the negative control, which registered an increase in tumor size of 88.87%. Noteworthy, the triple combination of cisplatin, WSR extract, and IF recorded the highest percentage in the size reduction (100%) and curable rate (100%). Besides, the combination of WSR extract and IF recorded the lowest percentage of size reduction (60.52%) among the combination treatments, along with a curable rate of 50%. The combination of WSR extract and cisplatin registered a reduction in tumor size of 81.12% with a curable rate of 50%. As observed, the same treatments were applied to EMT6/CPR cells. Tumor size was reduced remarkably (p < 0.05) for all treated groups as opposed to the negative control, which showed an increase in tumor size of 60.02% from the initial tumor size. Interestingly, combination treatments had higher tumor size reduction than single treatments. Regarding triple treatment, it registered a complete reduction in tumor size (100%); therefore, there were no mice with detectable tumors (100%). On the flip side, the WSR extract and cisplatin combination exhibited a higher reduction in tumor size than the WSR extract and IF combination (69.49 and 53.36%, consequently), besides the same curable rate (66.66%)."

https://www.frontiersin.org/articles/10.3389/fnut.2022.863619/full


   
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MAT as a promising therapeutic strategy against triple-negative breast cancer via inhibiting PI3K/AKT pathway

https://www.nature.com/articles/s41598-023-39655-9

"Matrine (MAT) is an alkaloid extracted from Sophora flavescens. It has good anticancer effects, and thus can be explored as a new therapeutic agent in TNBC research. We performed bioinformatics analysis to analyze the differentially expressed genes between normal breast tissues and TNBC tissues, and comprehensive network pharmacology analyses. The activity and invasion ability of TNBC cells treated with MAT were analyzed. Apoptosis and cell cycle progression were determined using cytometry. We used Monodansylcadaverine (MDC) staining to determine the condition of autophagosomes. Finally, the expression levels of the key target proteins of the PI3K/AKT pathway were determined using western blotting. The proliferation and invasion ability of MDA-MB-231 and MDA-MB-468 can be effectively inhibited by MAT. The results of flow cytometry indicated that MAT arrested the TNBC cell cycle and induced apoptosis. In addition, we confirmed that MAT inhibited the expression of BCL-2 while up-regulating the expression of cleaved caspase-3. Moreover, enhanced intensity of MDC staining and high LC3-II expression were observed, which confirmed that MAT induced autophagy in TNBC cells. Western blotting showed that MAT inhibited the PI3K/AKT pathway and downregulated the expressions of PI3K, AKT, p-AKT, and PGK1. This study provides feasible methods, which include bioinformatics analysis and in vitro experiments, for the identification of compounds with anti-TNBC properties. MAT inhibited the PI3K/AKT signaling pathway, arrested cell cycle, as well as promoted cell apoptosis and autophagy. These experiments provide evidence for the anti-TNBC effect of MAT and identified potential targets against TNBC."


   
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Naringenin in combination with quercetin/fisetin shows synergistic anti-proliferative and migration reduction effects in breast cancer cell lines

https://link.springer.com/article/10.1007/s11033-023-08664-2

"Conclusion: Our results indicate that quercetin/fisetin enhances the anti-proliferative and anti-migratory activities in combination with naringenin in MCF7 and MDA-MB-231 human breast cancer cell lines. Therefore, the combination of Que/Fis and Nar can be proposed as a promising therapeutic strategy for further investigations."


   
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Naringenin in combination with quercetin/fisetin shows synergistic anti-proliferative and migration reduction effects in breast cancer cell lines

https://link.springer.com/article/10.1007/s11033-023-08664-2

"Conclusion: Our results indicate that quercetin/fisetin enhances the anti-proliferative and anti-migratory activities in combination with naringenin in MCF7 and MDA-MB-231 human breast cancer cell lines. Therefore, the combination of Que/Fis and Nar can be proposed as a promising therapeutic strategy for further investigations."

Following oral administration, naringin is metabolised to the active metabolite naringenin and their hydroxylated, hydrogenated, dehydrogenated, and acetylated metabolites by intestinal microflora
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7118210

 


   
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updated synergies diagram


   
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Ammonia Drives Dendritic Cells into Dysfunction

"Ammonia levels are often elevated in patients with cirrhosis or tumors. Patients with these diseases are immunocompromised. In this study, we investigated the effects of ammonia on a member of the immune cell family, the dendritic cells (DCs). Our results demonstrated that ammonia diminished cell count, phagocytosis, and lymphocyte stimulation of DCs. Ammonia also induced DC swelling, excessive reactive oxygen species production, and mitochondrial damage, which may constitute the underlying mechanism of ammonia-induced DC dysfunction. In ammonium chloride (NH4Cl)–loaded mice, DCs exhibited lowered phagocytosis and a weakened immune response to the chicken OVA vaccine. DCs from patients with cirrhosis or ammonia-treated healthy human blood both exhibited diminished phagocytosis. Moreover, tumor cell conditioned medium drove DCs into dysfunction, which could be reversed by ammonia elimination. In a murine colon carcinoma model, we found that ammonia could regulate tumor growth involving DCs and their related immune response. These findings reveal that ammonia could drive DCs into dysfunction, which contributes to the immunocompromised state of patients with cirrhosis or tumors."

https://journals.aai.org/jimmunol/article/193/3/1080/108756/Ammonia-Drives-Dendritic-Cells-into-Dysfunction


   
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PRMT5 triggers glucocorticoid-induced cell migration in triple-negative breast cancer

https://www.life-science-alliance.org/content/6/10/e202302009

Early TNBC patients treated with chemo-immunotherapy combination in the neoadjuvant setting often need long-term steroid treatments to reduce the adverse effects from the multi-drug regimen. However, the prognostic impact of this GC intake on survival has been poorly explored. Given our data and the potential risk of metastatic progression, the routine premedication prescription of GCs for early TNBC patients has to be further assessed in prospective clinical trials for its reevaluation.


   
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An autocrine inflammatory forward-feedback loop after chemotherapy withdrawal facilitates the repopulation of drug-resistant breast cancer cells

https://www.nature.com/articles/cddis2017319

Abstract

Stromal cells, infiltrating immune cells, paracrine factors and extracellular matrix have been extensively studied in cancers. However, autocrine factors produced by tumor cells and communications between autocrine factors and intracellular signaling pathways in the development of drug resistance, cancer stem-like cells (CSCs) and tumorigenesis have not been well investigated, and the precise mechanism and tangible approaches remain elusive. Here we reveal a new mechanism by which cytokines produced by breast cancer cells after chemotherapy withdrawal activate both Wnt/β-catenin and NF-κB pathways, which in turn further promote breast cancer cells to produce and secrete cytokines, forming an autocrine inflammatory forward-feedback loop to facilitate the enrichment of drug-resistant breast cancer cells and/or CSCs. Such an unexpected autocrine forward-feedback loop and CSC enrichment can be effectively blocked by inhibition of Wnt/β-catenin and NF-κB signaling. It can also be diminished by IL8-neutralizing antibody or blockade of IL8 receptors CXCR1/2 with reparixin. Administration of reparixin after chemotherapy withdrawal effectively attenuates tumor masses in a human xenograft model and abolishes paclitaxel-enriched CSCs in the secondary transplantation. These results are partially supported by the latest clinical data set. Breast cancer patients treated with chemotherapeutic drugs exhibited poor survival rate (66.7 vs 282.8 months, P=0.00071) and shorter disease-free survival time if their tumor samples expressed high level of IL8, CXCR1, CXCR2 genes and Wnt target genes. Taken together, this study provides new insights into the communication between autocrine niches and signaling pathways in the development of chemotherapy resistance and CSCs; it also offers a tangible approach in breast cancer treatment.

"After exposure of untreated cells to paclitaxel-derived supernatants for 4 days, both CD44high/CD24-/low and ALDH-positive subpopulations in SUM149 and MDA-MB-231 cells (triple negative breast cancer – TNBC), and SUM190 (inflammatory breast cancer) cells increased significantly by 2-3 fold (Figure 1b; Supplementary Figure 1, flow cytometry). A marked upregulation of ALDH1, CD44 and OCT4 proteins were also observed (Figure 1c, western blot). As CD44high/CD24-/low and/or ALDH1 have been commonly used in the characterization of breast CSCs,16, 19, 20, 21 these results suggest that some factors produced by breast cancer cells themselves (i.e., autocrine factors) after drug withdrawal facilitate CSC enrichment."

"After analysis of the METABRIC data set,24 we found that among TNBC patients treated with chemotherapeutic drugs, samples with increased expression of Wnt/β-catenin target genes and NF-kB target genes exhibited poor survival rate and shorter disease-free time as compared with samples that expressed lower levels of these genes (Figure 2f). Together, our in vitro results and the clinical data analysis suggest that chemotherapeutic treatment may lead to enhanced secretion of inflammatory cytokines that can activate inflammatory pathways in the same line of breast cancer cells, which correlates positively with enhanced CSC phenotypes and poor clinical outcomes."

"After further analyzing the recently available clinical data set containing chemotherapeutic information (breast cancer TCGA, cBioPortal, Nature Communications 2016), we found that TNBC patients treated with chemotherapeutic drugs exhibited poor survival rate (66.7 vs 282.8 months, P=0.00071) and shorter disease-free survival time (P=0.00208) if tumor samples expressed higher levels of IL8, CXCR1, CXCR2 and the Wnt target genes than those expressed lower levels (Figure 4b). These clinical data suggest a tangible correlation between IL8/IL8 receptors, Wnt target genes and breast cancer progression after chemotherapy."

 

 


   
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Combination therapy shows promise in treatment of chemo-resistant breast cancer

https://hub.jhu.edu/2014/12/10/breast-cancer-treatment-protein-inhibitor/

"Treatment with digoxin plus a different chemotherapy drug, gemcitabine, brought tumor volumes to zero within three weeks and prevented the immediate relapse at the end of treatment that was seen in mice treated with gemcitabine alone."


   
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Posted by: @j

Combination therapy shows promise in treatment of chemo-resistant breast cancer

https://hub.jhu.edu/2014/12/10/breast-cancer-treatment-protein-inhibitor/

"Treatment with digoxin plus a different chemotherapy drug, gemcitabine, brought tumor volumes to zero within three weeks and prevented the immediate relapse at the end of treatment that was seen in mice treated with gemcitabine alone."

 


   
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pathways diagram updated


   
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Is Lactate an Oncometabolite? Evidence Supporting a Role for Lactate in the Regulation of Transcriptional Activity of Cancer-Related Genes in MCF7 Breast Cancer Cells https://pubmed.ncbi.nlm.nih.gov/32010625/

  • lactate alters the transcriptional activity of several key oncogenes as well as other driver genes
    involved in metabolic reprogramming as well as the regulation of cell cycle and proliferation.
  • glucose-derived lactate is sufficient to alter the transcriptional activity of key oncogenes, transcription factor genes, tumor suppressor genes as well as cell cycle, and proliferation genes.
  • while lactate is a metabolic intermediate, it has numerous downstream effects such as, metabolic reprogramming, and lactylation. The downstream effects of lactate in cancer remain to be determined.
  • Our results showing an effect of lactate on expressions of MYC and HIF1A genes are consistent with results of others showing upregulation of the glycolytic pathway in cancer. Hence, our results obtained on transcription of MYC and HIFA are supportive of our lactogenesis hypothesis.
  • we found that all CDKs were overexpressed by lactate exposure in a range from 2- to 6.7-fold
  • lactate signals multiple key steps essential in carcinogenesis, including cell proliferation.

Although lactate has been historically associated with exercise, it is noteworthy to differentiate between the effects of transient increases in exercise-derived lactate and chronic lactate elevation in cancer. During and after exercise, lactate is ultimately cleared from muscle fibers with the clearance rate depending on mitochondrial function and cardiometabolic fitness level of the person. In contrast, in cancer, lactate is not rapidly cleared, and is highly concentrated in the tumor and its microenvironment; an effect of which could be to promote carcinogenesis.


   
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L-Carnitine Decreases Her-2/neu in Breast Cancer Patients Treated with Tamoxifen

https://www.iosrjournals.org/iosr-jpbs/papers/Vol5-issue2/O0529198.pdf

 


   
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Posted by: @j

Is Lactate an Oncometabolite? Evidence Supporting a Role for Lactate in the Regulation of Transcriptional Activity of Cancer-Related Genes in MCF7 Breast Cancer Cells https://pubmed.ncbi.nlm.nih.gov/32010625/

  • lactate alters the transcriptional activity of several key oncogenes as well as other driver genes
    involved in metabolic reprogramming as well as the regulation of cell cycle and proliferation.
  • glucose-derived lactate is sufficient to alter the transcriptional activity of key oncogenes, transcription factor genes, tumor suppressor genes as well as cell cycle, and proliferation genes.
  • while lactate is a metabolic intermediate, it has numerous downstream effects such as, metabolic reprogramming, and lactylation. The downstream effects of lactate in cancer remain to be determined.
  • Our results showing an effect of lactate on expressions of MYC and HIF1A genes are consistent with results of others showing upregulation of the glycolytic pathway in cancer. Hence, our results obtained on transcription of MYC and HIFA are supportive of our lactogenesis hypothesis.
  • we found that all CDKs were overexpressed by lactate exposure in a range from 2- to 6.7-fold
  • lactate signals multiple key steps essential in carcinogenesis, including cell proliferation.

Although lactate has been historically associated with exercise, it is noteworthy to differentiate between the effects of transient increases in exercise-derived lactate and chronic lactate elevation in cancer. During and after exercise, lactate is ultimately cleared from muscle fibers with the clearance rate depending on mitochondrial function and cardiometabolic fitness level of the person. In contrast, in cancer, lactate is not rapidly cleared, and is highly concentrated in the tumor and its microenvironment; an effect of which could be to promote carcinogenesis.

 

The effect of Coenzyme Q10 supplementation on serum levels of lactate, pyruvate, matrix metalloproteinase 9 and nitric oxide in women with migraine. A double-blind, placebo, controlled randomized clinical trial

https://www.sciencedirect.com/science/article/abs/pii/S1876382018303767

"Treatment with CoQ10 significantly reduced serum concentrations of lactate, pyruvate, MMP-9 and NO while CoQ10 concentrations increased after 12 weeks (p < 0.05). There was a significant reduction in lactate/pyruvate ratio in intervention group. None of these changes had been observed in placebo treated group (p > 0.05). "

 


   
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(@j)
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Posted by: @j

Is Lactate an Oncometabolite? Evidence Supporting a Role for Lactate in the Regulation of Transcriptional Activity of Cancer-Related Genes in MCF7 Breast Cancer Cells https://pubmed.ncbi.nlm.nih.gov/32010625/

  • lactate alters the transcriptional activity of several key oncogenes as well as other driver genes
    involved in metabolic reprogramming as well as the regulation of cell cycle and proliferation.
  • glucose-derived lactate is sufficient to alter the transcriptional activity of key oncogenes, transcription factor genes, tumor suppressor genes as well as cell cycle, and proliferation genes.
  • while lactate is a metabolic intermediate, it has numerous downstream effects such as, metabolic reprogramming, and lactylation. The downstream effects of lactate in cancer remain to be determined.
  • Our results showing an effect of lactate on expressions of MYC and HIF1A genes are consistent with results of others showing upregulation of the glycolytic pathway in cancer. Hence, our results obtained on transcription of MYC and HIFA are supportive of our lactogenesis hypothesis.
  • we found that all CDKs were overexpressed by lactate exposure in a range from 2- to 6.7-fold
  • lactate signals multiple key steps essential in carcinogenesis, including cell proliferation.

Although lactate has been historically associated with exercise, it is noteworthy to differentiate between the effects of transient increases in exercise-derived lactate and chronic lactate elevation in cancer. During and after exercise, lactate is ultimately cleared from muscle fibers with the clearance rate depending on mitochondrial function and cardiometabolic fitness level of the person. In contrast, in cancer, lactate is not rapidly cleared, and is highly concentrated in the tumor and its microenvironment; an effect of which could be to promote carcinogenesis.

 

illustration attached, shows the central role in cancer development of lactate

 


   
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Posted by: @j

Posted by: @j

Is Lactate an Oncometabolite? Evidence Supporting a Role for Lactate in the Regulation of Transcriptional Activity of Cancer-Related Genes in MCF7 Breast Cancer Cells https://pubmed.ncbi.nlm.nih.gov/32010625/

  • lactate alters the transcriptional activity of several key oncogenes as well as other driver genes
    involved in metabolic reprogramming as well as the regulation of cell cycle and proliferation.
  • glucose-derived lactate is sufficient to alter the transcriptional activity of key oncogenes, transcription factor genes, tumor suppressor genes as well as cell cycle, and proliferation genes.
  • while lactate is a metabolic intermediate, it has numerous downstream effects such as, metabolic reprogramming, and lactylation. The downstream effects of lactate in cancer remain to be determined.
  • Our results showing an effect of lactate on expressions of MYC and HIF1A genes are consistent with results of others showing upregulation of the glycolytic pathway in cancer. Hence, our results obtained on transcription of MYC and HIFA are supportive of our lactogenesis hypothesis.
  • we found that all CDKs were overexpressed by lactate exposure in a range from 2- to 6.7-fold
  • lactate signals multiple key steps essential in carcinogenesis, including cell proliferation.

Although lactate has been historically associated with exercise, it is noteworthy to differentiate between the effects of transient increases in exercise-derived lactate and chronic lactate elevation in cancer. During and after exercise, lactate is ultimately cleared from muscle fibers with the clearance rate depending on mitochondrial function and cardiometabolic fitness level of the person. In contrast, in cancer, lactate is not rapidly cleared, and is highly concentrated in the tumor and its microenvironment; an effect of which could be to promote carcinogenesis.

 

illustration attached, shows the central role in cancer development of lactate

 

Beta-Caryophyllene is an ART1 inhibitor

https://www.researchgate.net/figure/BCP-percentages-in-plants-and-foods_tbl1_350284549

 


   
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NFYA promotes malignant behavior of triple-negative breast cancer in mice through the regulation of lipid metabolism

https://www.nature.com/articles/s42003-023-04987-9

"Two splicing variants exist in NFYA that exhibit high expression in many human tumour types. The balance in their expression correlates with prognosis in breast cancer, but functional differences remain unclear. Here, we demonstrate that NFYAv1, a long-form variant, upregulates the transcription of essential lipogenic enzymes ACACA and FASN to enhance the malignant behavior of triple-negative breast cancer (TNBC). Loss of the NFYAv1-lipogenesis axis strongly suppresses malignant behavior in vitro and in vivo, indicating that the NFYAv1-lipogenesis axis is essential for TNBC malignant behavior and that the axis might be a potential therapeutic target for TNBC. Furthermore, mice deficient in lipogenic enzymes, such as Acly, Acaca, and Fasn, exhibit embryonic lethality; however, Nfyav1-deficient mice exhibited no apparent developmental abnormalities. Our results indicate that the NFYAv1-lipogenesis axis has tumour-promoting effects and that NFYAv1 may be a safe therapeutic target for TNBC."


   
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Triple negative breast cancer development can be selectively suppressed by sustaining an elevated level of cellular cyclic AMP through simultaneously blocking its efflux and decomposition

https://augusta.elsevierpure.com/en/publications/triple-negative-breast-cancer-development-can-be-selectively-supp

Triple negative breast cancer (TNBC) has the highest mortality among all breast cancer types and lack of targeted therapy is a key factor contributing to its high mortality rate. In this study, we show that 8-bromo-cAMP, a cyclic adenosine monophosphate (cAMP) analog at high concentration (>1 mM) selectively suppresses TNBC cell growth. However, commonly-used cAMP-elevating agents such as adenylyl cyclase activator forskolin and pan phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX) are ineffective. Inability of cAMP elevating agents to inhibit TNBC cell growth is due to rapid diminution of cellular cAMP through efflux and decomposition. By performing bioinformatics analyses with publically available gene expression datasets from breast cancer patients/established breast cancer cell lines and further validating using specific inhibitors/siRNAs, we reveal that multidrug resistance-associated protein 1/4 (MRP1/4) mediate rapid cAMP efflux while members PDE4 subfamily facilitate cAMP decomposition. When cAMP clearance is prevented by specific inhibitors, forskolin blocks TNBC's in vitro cell growth by arresting cell cycle at G1/S phase. Importantly, cocktail of forskolin, MRP inhibitor probenecid and PDE4 inhibitor rolipram suppresses TNBC in vivo tumor development. This study suggests that a TNBC-targeted therapeutic strategy can be developed by sustaining an elevated level of cAMP through simultaneously blocking its efflux and decomposition.


   
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in my view attached image illustrates how important it is to address ammonia in parallel to any intervention. 


   
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Tamoxifen and raloxifene suppress the proliferation of estrogen receptor-negative cells through inhibition of glutamine uptake

https://pubmed.ncbi.nlm.nih.gov/20383709/


   
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FOXO1 activates glutamine synthetase gene in mouse skeletal muscles through a region downstream of 3=-UTR: possible contribution to ammonia detoxification

https://nutrition.life.kpu.ac.jp/wp-content/uploads/2012/12/E485.full_.pdf

Insulin inhibits FOXO so it's possible high insulin compromises ammonia detoxification.


   
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Nrf3 promotes the proliferation and migration of triple‑negative breast cancer by activating PI3K/AKT/mTOR and
epithelial‑mesenchymal transition

https://www.spandidos-publications.com/10.3892/ol.2023.14030/abstract


   
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Nrf3 promotes the proliferation and migration of triple‑negative breast cancer by activating PI3K/AKT/mTOR and
epithelial‑mesenchymal transition

https://www.spandidos-publications.com/10.3892/ol.2023.14030/abstract

Context appears crucial regarding the NRF3 transcription factor: Nrf3 Functions Reversely as a Tumorigenic to an Antitumorigenic Transcription Factor in Obese Mice

https://www.jstage.jst.go.jp/article/tjem/259/1/259_2022.J090/_html/-char/en

Nrf3 knockdown decreased tumor growth in mice fed a normal diet (ND), whereas it reversely increased tumor growth in mice fed a high-fat diet (HFD). 

 

 


   
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Advances in immunotherapy for triple-negative breast cancer

https://molecular-cancer.biomedcentral.com/articles/10.1186/s12943-023-01850-7


   
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A very interesting study: PDE5 inhibitors enhance Celecoxib killing in multiple tumor types.

https://onlinelibrary.wiley.com/doi/10.1002/jcp.24843 (you can use https://sci-hub.se/ to read it)


   
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@j I started taking Cialis about 2 months ago.


   
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" Our data also showed that AKG supplementation inhibited the glycolysis pathway as indicated by decreased mRNA expression of phosphofructokinase (Pfkl), aldolase fructose-bisphosphate A (Aldoa), and lactate dehydrogenase A (Ldha) (fig. S1L). "

https://www.science.org/doi/10.1126/sciadv.abn2879


   
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A Positive Feedback Loop Between TGFβ and Androgen Receptor Supports Triple-negative Breast Cancer Anoikis Resistance

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7806239/


   
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