Publications by authors named "G Goodwin Jinesh"
Article Synopsis
- The chromosome-19 miRNA cluster (C19MC) plays a role in how certain viruses affect multinucleated cells in the placenta, but its connection to multinucleation was previously unclear.
- Researchers found that C19MC is linked to meiosis-related genes and discovered a new process called meiosis-III, where nuclear division and cell division happen together to create multinucleated cells.
- The study shows that C19MC is crucial for a structure called nucle(ol)ar invasive cytoplasm (NiC) which helps in the division of nuclei and supports the creation of multinucleated cells, providing insights for cancer research, virus interactions, and potential therapies.
Metastasis is a pivotal event that accelerates the prognosis of cancer patients towards mortality. Therapies that aim to induce cell death in metastatic cells require a more detailed understanding of the metastasis for better mitigation. Towards this goal, we discuss the details of two distinct but overlapping pathways of metastasis: a classical reversible epithelial-to-mesenchymal transition (hybrid-EMT)-driven transport pathway and an alternative cell death process-driven blebbishield metastatic-witch (BMW) transport pathway involving reversible cell death process.
View Article and Find Full Text PDFA subset of hepatocellular carcinoma (HCC) overexpresses the chromosome 19 miRNA cluster (C19MC) and is associated with an undifferentiated phenotype marked by overexpression of cancer testis antigens (CTAs) including anti-apoptotic melanoma-A antigens (MAGEAs). However, the regulation of C19MC miRNA and MAGEA expression in HCCs are not understood. Here we show that, C19MC overexpression is tightly linked to a sub-set of HCCs with transcription-incompetent p53.
View Article and Find Full Text PDFCellular transformation is a major event that helps cells to evade apoptosis, genomic instability checkpoints, and immune surveillance to initiate tumorigenesis and to promote progression by cancer stem cell expansion. However, the key molecular players that govern cellular transformation and ways to target cellular transformation for therapy are poorly understood to date. Here we draw key evidences from the literature on K-Ras-driven cellular transformation in the context of apoptosis to shed light on the key players that are required for cellular transformation and explain how aiming p53 could be useful to target cellular transformation.
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