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A Novel Role for the Tumor Suppressor Gene in Tumorigenesis and Chemotherapy Response. | LitMetric

AI Article Synopsis

  • - The study investigates how platinum-based chemotherapy, although standard for treating epithelial tumors, can lead to resistance, focusing on cytogenetic changes in lung and ovarian cancer cell lines after cisplatin treatment.
  • - Researchers utilized various methods, including microarrays and RNA-sequencing, to discover gene alterations related to cancer development, finding that certain genes are frequently deleted or downregulated, which impacts tumor response to chemotherapy.
  • - Results indicate that targeting specific genes associated with the Wnt-signaling pathway may offer new therapeutic strategies for overcoming cisplatin resistance in tumors, including evidence that lower expression of these genes correlates with better survival in lung cancer patients.

Article Abstract

Despite often leading to platinum resistance, platinum-based chemotherapy continues to be the standard treatment for many epithelial tumors. In this study we analyzed and validated the cytogenetic alterations that arise after treatment in four lung and ovarian paired cisplatin-sensitive/resistant cell lines by 1-million microarray-based comparative genomic hybridization (array-CGH) and qRT-PCR methodologies. RNA-sequencing, functional transfection assays, and gene-pathway activity analysis were used to identify genes with a potential role in the development of this malignancy. The results were further explored in 55 lung and ovarian primary tumors and control samples, and in two extensive in silico databases. Long-term cell exposure to platinum induces the frequent deletion of gene. Its expression re-sensitized tumor cells to platinum and recovered the levels of Wnt/β-catenin transcriptional activity. expression was also frequently downregulated in epithelial tumors, predicting a worse overall survival. We also identified an inverse correlation between and expression, revealing that Non-small cell lung cancer (NSCLC) patients with lower expression of had a better overall survival rate. We defined the implication of as a molecular mechanism behind the development of cisplatin resistance probably through the activation of the Wnt-signaling pathway. This data highlights the possible role of and as novel therapeutic targets for platinum resistant tumors.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7226299PMC
http://dx.doi.org/10.3390/cancers12040786DOI Listing

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