scispace - formally typeset
Search or ask a question

What cause the decrease expression of hormone receptor during triple negative breast cancer development? 


Best insight from top research papers

The decrease in hormone receptor expression during the development of triple negative breast cancer (TNBC) is caused by various factors. One possible cause is the inhibition of growth hormone receptor (GHR) expression, which is associated with a worse outcome in TNBC . Another factor is the disturbance of proper estrogen signaling, which is directly associated with TNBC risk . Additionally, the expression of the inhibitory peptide and receptor in the opioid growth factor (OGF) - opioid growth factor receptor (OGFr) axis is reduced in TNBC, diminishing the efficacy of this regulatory pathway . Furthermore, the androgen receptor (AR) plays a role in a subset of TNBC, and inhibiting AR activity decreases proliferation and tumor burden . These factors contribute to the decrease in hormone receptor expression observed in TNBC.

Answers from top 5 papers

More filters
Papers (5)Insight
The paper does not provide information on the cause of decreased hormone receptor expression during triple negative breast cancer development.
The paper does not provide information on the specific cause of the decreased expression of hormone receptors during triple negative breast cancer development.
The paper does not provide information on the specific causes of decreased hormone receptor expression during triple negative breast cancer development.
Open accessJournal Article
Comănescu M, A Potecă, C Cocosila, T. Poteca 
3 Citations
The paper does not provide information on the specific causes of decreased expression of hormone receptors during triple negative breast cancer development.
The paper does not provide information on the specific cause of decreased hormone receptor expression during triple negative breast cancer development.

Related Questions

What suppresses gene expression of estrogen receptor in breast cancer?4 answersEstrogen receptor (ER) gene expression is suppressed in breast cancer by multiple factors. One study found that disruption of ERα signaling led to the recruitment of polycomb repressors and histone deacetylases, resulting in stable repression of the progesterone receptor (PR) gene, a known ERα target. Another study showed that CD73 expression, which is regulated by estrogen signaling, was significantly lower in ER(+) breast cancers compared to ER(-) tumors. Additionally, mutations in ER were found to impact the expression of thousands of genes, including those not typically regulated by wildtype ER, suggesting post-transcriptional effects. Furthermore, PARP-1 was found to regulate estrogen-dependent transcription in ERα-positive breast cancers, influencing the expression of estrogen-regulated genes. Finally, loss of expression of the Checkpoint with FHA and Ring Finger (CHFR) gene, potentially due to promoter hypermethylation, was associated with decreased CHFR protein expression and increased tumor size in breast cancer.
Does TGFB contribute to the development of triple-negative breast cancer?5 answersTGFB contributes to the development of triple-negative breast cancer. TGFB1 is a multi-functional cytokine that regulates mammary gland development and cancer progression. Increased expression of TGFB1 is associated with an increased breast cancer risk. TGFB-β signaling plays an important role during metastasis of breast cancer, and it is involved in the regulation of breast cancer stem cells. Rab1B, a member of the RAS oncogene family, acts as a metastasis suppressor in triple-negative breast cancer through regulating the TGF-β/Smad signaling pathway. Deregulation of the TGF-β signaling pathway is commonly seen in cancer, including breast cancer.
What are the potential roles of lncRNAs and miRNAs in triple-negative breast cancer?5 answersLong non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have potential roles in triple-negative breast cancer (TNBC). LncRNAs have been identified as drivers of TNBC progression and can be targeted using RNA therapeutics to reduce systemic toxicities. LncRNAs also interact with miRNAs, modulating their action and potentially impacting tumor resistance to chemotherapeutic drugs. Abnormal expression of lncRNAs affects the tumor immune microenvironment in breast cancer, suggesting their potential as targets for immunotherapy. Additionally, lncRNAs MACC1-AS1 and UCA1 have been found to interact with multiple miRNAs, mediating the expression of different genes and affecting cancer cell growth. These findings highlight the importance of lncRNAs and miRNAs in TNBC, both as potential therapeutic targets and as regulators of gene expression and tumor behavior.
What is the role of Wnt signaling in cancer stem cells in triple-negative breast cancer?5 answersWnt signaling plays a crucial role in cancer stem cells (CSCs) in triple-negative breast cancer (TNBC). Aberrant activation of the Wnt/β-catenin pathway contributes to the self-renewal, metastasis, and resistance to therapy in TNBC. Studies have shown that the Wnt/β-catenin pathway is involved in the regulation of CSCs in TNBC, which are responsible for cancer initiation, therapy resistance, and disease progression. The Wnt/β-catenin pathway interacts with other signaling pathways, such as receptor tyrosine kinase (RTK) signaling, NF-κB pathway, and cholesterol biosynthesis pathway, to promote CSC proliferation, survival, and differentiation. Targeting the Wnt/β-catenin pathway, in combination with standard therapies, has the potential to improve the prognosis of TNBC patients by inhibiting CSC function and reducing tumor growth and metastasis.
What is the role of Wnt signaling in triple-negative breast cancer?5 answersAberrant Wnt signaling plays a crucial role in triple-negative breast cancer (TNBC). It is responsible for self-renewal, metastasis, resistance to apoptosis and chemotherapy, and induction of epithelial-mesenchymal transition (EMT) and metastasis. Dysregulation of the Wnt/β-catenin pathway promotes TNBC by regulating the expression of downstream target genes involved in proliferation, stemness, and metastasis. In addition to the Wnt/β-catenin pathway, other Wnt signaling pathways, such as Wnt-planar cell polarity (PCP) and Wnt-Ca2+ signaling, also contribute to the progression of TNBC. The dysregulation of these pathways leads to the activation of β-catenin and downstream target genes, promoting invasion, neovascularization, and aggressiveness of TNBC tumors. Understanding the role of Wnt signaling in TNBC is crucial for the development of targeted therapies that can inhibit the pathway and overcome resistance to current treatments.
Show papers on TRIPLE NEGATIVE BREAST CANCER?5 answersTriple-negative breast cancer (TNBC) is a subtype of breast cancer that lacks hormone receptors and HER2 gene amplification. It represents about 15-20% of all breast cancers and is known for its aggressive nature and poor prognosis compared to other forms of breast cancer. TNBC can be accurately diagnosed using mammography, ultrasound, and MRI, with MRI being the most sensitive modality. Recent advancements in the management of metastatic TNBC include the incorporation of immune checkpoint inhibitors with chemotherapy and the development of novel antibody-drug conjugates with new targets. Understanding the tumor-immune microenvironment and molecular vulnerabilities in TNBC has led to significant strides in treatment options. Radiation therapy plays a crucial role in the treatment of TNBC, with postoperative radiation therapy recommended for most patients and specific indications based on tumor characteristics. Future studies should evaluate the indications of radiation therapy in the context of novel systemic treatments.

See what other people are reading

Does the Mediterranean diet or ketogenic diet help with breast cancer and diabetes?tment?
5 answers
Does the Mediterranean diet or ketogenic diet help with breast cancer and diabetes?tment?
5 answers
How does TNBC spread?
5 answers
How does TNBC spread?
5 answers
What is SIRT1 signal cascade?
5 answers
The SIRT1 signal cascade involves various pathways and interactions that play crucial roles in different physiological processes. SIRT1 is implicated in regulating inflammation, stress resistance, and cell death pathways, such as pyroptosis. It also influences Wnt signaling by interacting with Dishevelled proteins, impacting gene expression and cell migration. In the context of brain reward regions, SIRT1 and SIRT2 are involved in behavioral responses to drugs of abuse, like cocaine and morphine, through histone modifications and synaptic protein regulation. Additionally, in the context of bronchopulmonary dysplasia (BPD), SIRT1-related signaling pathways are linked to mitochondrial dysfunction, inflammation, apoptosis, and fibrosis, highlighting its role in disease pathogenesis and potential therapeutic targets. These diverse roles underscore the complexity and significance of the SIRT1 signal cascade in various biological contexts.
Has estrogen an anti or proinflammatory effect?
4 answers
Estrogen exhibits predominantly anti-inflammatory effects in various contexts. Studies highlight that estrogen plays a crucial role in mitigating inflammation through different mechanisms. Research indicates that estrogen can ameliorate inflammation by inhibiting the NF-κB pathway and reducing the expression of pro-inflammatory mediators. Additionally, estrogen has been shown to enhance bacterial clearance through phagocytosis, particularly mediated by ER-α. The presence of specific estrogen receptors, such as ER-α 36-kDa splice variant and GPR30, further supports estrogen's anti-inflammatory actions by inhibiting NF-κB transcriptional activity. Overall, the data suggests that estrogen's anti-inflammatory properties are significant and can potentially be leveraged for therapeutic interventions in conditions associated with inflammation.
How to modulate the expression of SOCS molecules in cancers?
5 answers
To modulate the expression of SOCS molecules in cancers, various approaches have been explored. Epigenetic regulation plays a crucial role in controlling SOCS expression. For instance, SOCS1 methylation levels were significantly higher in hepatocellular carcinoma (HCC) compared to non-tumoral tissues, and treatment with 5-Azacytidine reduced DNMT1 expression and modulated SOCS1 levels in different HCC cell subtypes. Additionally, SOCS1 has been implicated in regulating cellular responses to radiation in colorectal cancer cells, where over-expression of SOCS1 promoted radiation-induced apoptosis by inhibiting Jak3/STAT3 and Erk activities. Moreover, SOCS1's interaction with p53 and its ability to regulate cellular senescence depend on specific structural motifs, with phosphorylation of SOCS1 by SRC family kinases inhibiting its tumor-suppressive activity. These findings suggest that targeting epigenetic modifications and signaling pathways could be potential strategies to modulate SOCS expression in cancer.
Cancer-associated fibroblasts rewire the estrogen receptor response in luminal breast cancer, enabling estrogen independence
5 answers
Cancer-associated fibroblasts (CAFs) play a crucial role in rewiring the estrogen receptor (ER) response in luminal breast cancer, influencing estrogen independence. CAFs consist of distinct subtypes, with CD146-negative (CD146neg) CAFs suppressing ER expression, reducing estrogen sensitivity, and promoting tamoxifen resistance, while CD146-positive (CD146pos) CAFs maintain ER expression and enhance sensitivity to tamoxifen. Additionally, CAFs respond to estrogen through the GPR30 receptor, inducing signaling pathways that impact gene expression related to cell proliferation and migration. A 5-gene CAF risk signature, including RIN2, THBS1, IL1R1, RAB31, and COL11A1, has been identified to predict prognosis and therapeutic outcomes in luminal breast cancer, highlighting the significant influence of CAF-related factors on treatment response and patient outcomes.
Does androgen receptor change after therapy with CDK4/6i?
5 answers
After therapy with CDK4/6 inhibitors (CDK4/6i), there is evidence of changes in the androgen receptor (AR). Studies have shown that CDK4/6 inhibition is effective in models of treatment-resistant prostate cancer, including those expressing AR mutants or lacking AR expression. In ER+ breast cancer, combining AR agonists with CDK4/6i has demonstrated potent and durable inhibition of tumor growth, indicating an interaction between AR and CDK4/6 signaling pathways. Additionally, the combination of a selective androgen receptor modulator (SARM) or a natural AR ligand with CDK4/6i has shown enhanced AR signaling and upregulation of an AR gene signature associated with better prognosis in preclinical models of CDK4/6i-resistant breast cancer. Therefore, therapy with CDK4/6i can impact AR expression and signaling pathways in both prostate and breast cancers.
What are PITX2 and ZFHX3?
4 answers
PITX2 is a gene associated with organogenesis and cancer progression, particularly in head and neck squamous cell carcinoma (HNSC). It plays a role in DNA binding and transcription, impacting HNSC prognosis and immune cell regulation. On the other hand, ZFHX3, also known as ATBF1, is a zinc-finger homeodomain transcription factor crucial for brain development and function. Loss-of-function variants in ZFHX3 are linked to syndromic intellectual disability, growth issues, and facial characteristics like cleft palate. In prostate cancer, ZFHX3 interacts with the m6A modification enzyme FTO, affecting cell proliferation and tumorigenesis. Additionally, reduced ZFHX3 expression in prostate cancer leads to increased sensitivity to androgen receptor inhibitors, influencing tumor suppressor functions.
What is castration resistant prostrate cancer?
5 answers
Castration-resistant prostate cancer (CRPC) is a form of advanced prostate cancer that no longer responds to castration alone and becomes sensitive to androgen stimulation. It is characterized by the progression of the disease despite androgen deprivation therapy (ADT), leading to high mortality rates. Changes in PSMA expression and imaging findings play a crucial role in diagnosing CRPC, with higher PSMA expression observed in metastatic CRPC compared to metastatic hormone-sensitive prostate cancer (mCSPC). The development of CRPC involves complex mechanisms, including aberrant activation of androgen receptor signaling, non-coding RNAs, and alternative steroidogenesis pathways, contributing to treatment resistance. Accurate imaging modalities like Ga-68-PSMA-11 PET/CT are essential for detecting CRPC progression and guiding targeted therapies.