scispace - formally typeset
Search or ask a question

What is the molecular mechanism of HSD3B1 in ovarian cancer development and progression? 


Best insight from top research papers

HSD3B1 plays a crucial role in ovarian cancer development and progression. In ovarian cancer, overexpression of HSD3B1 is associated with poor prognosis, promoting cell proliferation, migration, and invasion through activation of the Wnt/β-catenin signaling pathway. Additionally, HSD3B1 is involved in the dysregulation of pathways such as the cell cycle, p53 signaling, and drug metabolism, indicating its significance in ovarian cancer progression. The HSD3B1 gene variant, particularly the 1245A>C polymorphism, leads to increased androgen synthesis, potentially impacting the response to hormonal therapies in ovarian cancer. Understanding the molecular mechanisms of HSD3B1 in ovarian cancer sheds light on potential therapeutic targets and prognostic indicators for this challenging disease.

Answers from top 5 papers

More filters

Related Questions

What are the potential mechanisms underlying the association between CHD1 gene mutations and the development of gastric cancer?5 answersMutations in the CHD1 gene, encoding E-cadherin, are linked to the development of gastric cancer through various mechanisms. These mutations, commonly truncating variants, lead to loss of E-cadherin function, promoting cellular dedifferentiation and poor prognosis in hereditary diffuse gastric cancer (HDGC). The loss of E-cadherin initiates HDGC by deregulating developmental transcriptional programs, shifting cell differentiation trajectories towards neoplastic lesions. Additionally, CHN1 gene upregulation in gastric cancer is associated with poor patient survival, immune cell infiltration, and involvement in cancer-related pathways, suggesting a pro-carcinogenic role potentially mediated by DNA methylation. These findings highlight the critical role of CHD1 mutations in gastric cancer progression and emphasize the need for further research to elucidate the molecular mechanisms driving this association.
What is the relationship between molecular subtypes and methylation status in ovarian cancer?5 answersThe molecular subtypes of ovarian cancer are intricately linked to the methylation status of the disease. Research has identified distinct methylation-based subgroups within ovarian cancer that exhibit significant survival differences, reflecting the heterogeneity of the disease. These subgroups provide valuable insights into the molecular underpinnings of ovarian cancer, shedding light on its etiology and prognosis. Furthermore, the methylation profiles have been associated with specific pathways like fatty acid metabolism and the extracellular matrix, highlighting the functional implications of methylation alterations in ovarian cancer. Additionally, the methylation status of various DNA repair genes has been linked to prognosis and therapy resistance in epithelial ovarian carcinoma, suggesting a potential role as predictive biomarkers for patient outcomes.
How does DEG analysis contribute to understanding the molecular mechanisms underlying ovarian cancer development and progression?5 answersDEG analysis plays a crucial role in understanding the molecular mechanisms underlying ovarian cancer development and progression. By identifying differentially expressed genes (DEGs) between ovarian cancer and control samples, researchers can gain insights into the genes and pathways that are dysregulated in the disease. Several studies have used DEG analysis to identify potential biomarkers for ovarian cancer, such as miRNAs and hub genes. These biomarkers can provide valuable information for cancer diagnosis, prognosis, and treatment strategies. DEG analysis also allows for the identification of key genes and biological processes associated with ovarian cancer. For example, DEG analysis has revealed genes involved in protein metabolism, histogenesis, and the development of reproductive and ocular tissues. Overall, DEG analysis contributes to a better understanding of the molecular mechanisms driving ovarian cancer and can aid in the development of targeted therapies and personalized medicine approaches.
What is the role of TIM3 in ovarian cancer?4 answersTIM-3 plays a role in ovarian cancer by being expressed in the tumor microenvironment and affecting the immune response. Higher expression of TIM-3 is associated with a more advanced tumor stage. TIM-3 expression is correlated with the activation of the Wnt/β-catenin signaling pathway, promoting malignant behaviors of tumor cells. In high-grade serous carcinoma (HGSC), TIM-3 expression is associated with functional exhaustion of CD8+ T cells and poor disease outcome. However, the impact of TIM-3 expression on patient stratification based on CD8+ T cell abundance is inconclusive. TIM-3-positive tissue-resident memory (Trm) T cells are identified in epithelial ovarian cancer (EOC) and are associated with improved patient survival. Combining TIM-3 blockade with PD-1 blockade may be a potential therapeutic strategy for reactivating anti-cancer immunity in EOC.
What is the mechanism of PARP in ovarian cancer?5 answersPoly (ADP-ribose) polymerase (PARP) inhibitors are targeted therapies for the treatment of ovarian cancer. PARP inhibitors interfere with DNA repair events, leading to cell death through a mechanism known as synthetic lethality. They have been approved as frontline treatment and have shown efficacy in BRCA1/BRCA2 mutant cancers. However, resistance to PARP inhibitors can develop, and understanding the underlying mechanisms is crucial for overcoming this resistance. Mechanisms of resistance include reversion of homologous repair deficiency (HRd) to homologous repair proficiency driven by epigenetic and genetic changes. Combination therapies that work synergistically with PARP inhibitors are being developed to restore drug sensitivity and overcome resistance. These combination therapies target replication stress, DNA repair pathways, and other cross-talk pathways. Efforts are also being made to identify and select patients for appropriate therapy or combination strategies.
What are the mechanisms by which BRCA mutations cause ovarian cancer?5 answersBRCA mutations cause ovarian cancer through various mechanisms. These mutations lead to defects in DNA repair mechanisms such as double strand DNA breaks (DSB) and non-homologous end joining (NHEJ). BRCA1 and BRCA2 genes are involved in maintaining genomic stability and are crucial for DNA damage repair via homologous recombination (HR). Mutations in these genes result in the accumulation of double-strand breaks, which can lead to tumorigenesis. The risk of developing ovarian cancer is significantly increased in women with BRCA1 and BRCA2 mutations. These mutations can be detected through genetic testing, allowing for the identification of individuals at high risk and the implementation of preventive strategies. Additionally, BRCA mutations confer sensitivity to DNA-damaging agents such as platinum chemotherapy and poly-ADP ribose polymerase inhibitors (PARPi). Understanding these mechanisms is crucial for diagnosis, prognosis, and targeted therapy in ovarian cancer.