4.6 Article

Elevated β-catenin activity contributes to carboplatin resistance in A2780cp ovarian cancer cells

期刊

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2015.10.138

关键词

Epithelial ovarian cancer; Wnt/beta-catenin; Carboplatin; Chemoresistance

资金

  1. Women and Children's Health Research Institute (WCHRI)
  2. Royal Alexandra Hospital Foundation (RAHF)
  3. WCHRI graduate studentship
  4. CIHR Master's Award: Frederick Banting and Charles Best Canada Graduate Scholarships
  5. MatCH program at the University of Alberta
  6. FOMD/AHS graduate studentship
  7. Medical Science Graduate Program Scholarship

向作者/读者索取更多资源

Ovarian cancer is the fifth leading cause of cancer-related mortalities in women. Epithelial ovarian cancer (EOC) represents approximately 90% of all ovarian malignancies. Most EOC patients are diagnosed at advanced stages and current chemotherapy regimens are ineffective against advanced EOC due to the development of chemoresistance. It is important to better understand the molecular mechanisms underlying acquired resistance to effectively manage this disease. In this study, we examined the expression of the Wnt/beta-catenin signaling components in the paired cisplatin-sensitive (A27805) and cisplatin-resistant (A2780cp) EOC cell lines. Our results showed that several negative regulators of Wnt signaling are downregulated, whereas a few Wnt ligands and known Wnt/beta-catenin target genes are upregulated in A2780cp cells compared to A2780s cells, suggesting that Wnt/beta-catenin signaling is more active in A2780cp cells. Further analysis revealed nuclear localization of beta-catenin and higher beta-catenin transcriptional activity in A2780cp cells compared to A2780s cells. Finally, we demonstrated that chemical inhibition of beta-catenin transcriptional activity by its inhibitor CCT036477 sensitized A2780cp cells to carboplatin, supporting a role for beta-catenin in carboplatin resistance in A2780cp cells. In conclusion, our data suggest that increased Wnt/beta-catenin signaling activity contributes to carboplatin resistance in A2780cp cells. (C) 2015 Elsevier Inc. All rights reserved.

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Takahiro Sasaki, Yoshiki Kuse, Shinsuke Nakamura, Masamitsu Shimazawa

Summary: PGRN deficiency plays a significant role in cardiac remodeling and arrhythmias post-myocardial infarction (MI), potentially by promoting metabolic abnormalities in macrophages.

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS (2024)

Article Biochemistry & Molecular Biology

Changes in myelinated nerve fibers induced by pulsed electrical stimulation: A microstructural perspective on the causes of electrical stimulation side effects

Hongwei Zhao, Yiqiang Li, Yibo Zhang, Chi Zhang

Summary: Electrical brain stimulation technology is commonly used to treat brain neurological disorders, but it can cause side effects. This study investigated the impact of electric fields on nerve fibers and revealed the possible origin of side effects. The findings provide guidance for selecting electrical parameters in clinical stimulation therapy.

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS (2024)

Article Biochemistry & Molecular Biology

Fatty acid elongation regulates mitochondrial 13-oxidation and cell viability in prostate cancer by controlling malonyl-CoA levels

Julia S. Scott, Lake-Ee Quek, Andrew J. Hoy, Johannes V. Swinnen, Zeyad D. Nassar, Lisa M. Butler

Summary: The fatty acid elongation enzyme ELOVL5 plays a critical role in promoting metastasis in prostate cancer. Knocking down ELOVL5 leads to the accumulation of malonyl-CoA, which inhibits fatty acid oxidation in mitochondria. This study highlights the importance of fatty acid elongation in regulating cell viability and provides a potential target for prostate cancer treatment.

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS (2024)

Article Biochemistry & Molecular Biology

The effects of noise exposure on hippocampal cognition in C57BL/6 mice via transcriptomics

Zan Zhou, Wen-jun Jiang, Li Li, Jun-qiang Si

Summary: This study investigates the effect of noise exposure on cognitive function in mice and explores the underlying molecular mechanisms. The findings suggest that noise exposure leads to increased inflammation, increased phosphorylation of Tau protein, and decreased levels of postsynaptic density protein, resulting in cognitive impairment.

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS (2024)