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Biology subjects

Murata, M. M.

Publications and source records attributed to Murata, M. M..

3 recordsLinked to original sources

A Practical Approach for Targeting Structural Variants Genome-wide in Plasma Cell-free DNA

Interrogating gene mutations and aberrant DNA methylation in plasma cell-free DNA (cfDNA) has become increasingly common for monitoring tumor burden in cancer patients. However, no tests currently target chromosomal structural variants (SVs) genome-wide. Here, we report a simple molecular and sequencing workflow, Genome-wide Analysis of Palindrome Formation (GAPF-seq), to probe DNA palindromes, a type of SV that often demarcates gene amplification. Low-coverage next-generation sequencing of palindrome-enriched DNA uncovered skewed chromosomal distributions of high-coverage 1-kb bins (HCBs) in tumor DNA. When combined with traditional machine learning, GAPF-seq differentiated 39 breast tumors from matched control DNA with an Area Under the Curve (AUC) of 0.955. A proof-of-concept liquid biopsy study using cfDNA from 27 prostate cancer patients and 24 control individuals yielded an average AUC of 0.896. HCBs on the X chromosome emerged as a nearly decisive feature and were linked to androgen receptor gene amplification. As a simple and agnostic liquid biopsy approach, GAPF-seq could fill this technological gap, offering unique cancer-specific SV profiles.

cancer biology↗

CitrusKB: A Comprehensive Knowledge Base for Transcriptome and Interactome of Citrus spp. Infected by Xanthomonas citri subsp. citri at Different Infection Stages

Citrus canker type A is a serious disease caused by Xanthomonas citri subsp. citri (X. citri), which is responsible for severe losses to growers and to the citrus industry worldwide. To date, no canker-resistant citrus genotypes are available, and there is limited information regarding the molecular and genetic mechanisms involved in the early stages of the citrus canker development. Here, we present the knowledge base for transcriptome of in vivo citrus interactome, the CitrusKB. This is the first in vivo interactome database for different citrus cultivars, and it was produced to provide a valuable source of information on citrus and their interaction with the citrus canker bacterium X. citri. The database provides tools for a user-friendly web interface to search and analyze a large amount of information regarding eight citrus cultivars with distinct levels of susceptibility to the disease and their interaction, at different stages of infection, with the citrus canker bacterium X. citri. Currently, CitrusKB comprises a reference citrus genome and its transcriptome, expressed transcripts, pseudogenes and predicted genomic variations (SNPs and SSRs). The updating process will continue by incorporating annotations and analysis tools. We expect that CitrusKB may substantially contribute to the area of citrus genomics. CitrusKB is accessible at http://bioinfo.deinfo.uepg.br/citrus. Users can download all the generated raw sequences and generated datasets by this study from the CitrusKB website.

genomics↗

Restoring p53 Function and Silencing REV3L Suppresses the Cancerous Metabolic Phenotype in Cisplatin Treated Human Non-Small Lung Carcinoma Cells

Lung cancer is one of the deadliest cancers in the world accounting for over one-quarter of all cancer-related deaths, but in many cases, the cancer can develop a resistance to the cisplatin-based chemotherapies. It is well known that cancer cells exhibit the Warburg effect and some studies have suggested that cancer cell metabolism may be linked to cisplatin resistance. In this study, the effects of tumor suppressor protein p53 and translesional synthesis protein REV3L are studied to relate DNA damage signaling and repair to cellular metabolism by using the fluorescence lifetime of the metabolic coenzyme NADH. It was found that simultaneously restoring function to p53 and silencing REV3L suppressed the cancerous metabolic phenotype and resulted in the greatest amount of cancer cell death. This study demonstrates a previously unrecognized relationship between p53 and REV3L in cellular metabolism and may lead to improvements in chemotherapy treatment plans that reduce cisplatin resistance in cancer cells.

cancer biology↗