Single-cell and spatial transcriptomics reveal cellular heterogeneity and immune niches in ovarian cancer drug resistance
DOI:
https://doi.org/10.61561/ssbgjms.v7i03.163Keywords:
Ovarian Cancer, Drug Resistance, Single-Cell RNA Sequencing, Spatial Transcriptomics, Tumor MicroenvironmentAbstract
Background: Ovarian cancer mortality remains high because of late diagnosis, recurrence, and treatment resistance. Bulk transcriptomics cannot resolve cell-specific resistance states or their spatial organization. This review examines how single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST) improve our understanding of the cellular and spatial mechanisms underlying drug resistance in ovarian cancer.
Methods: We narratively reviewed recent literature on ovarian cancer, platinum and PARP inhibitor resistance, immune low-response phenotypes, scRNA-seq, ST, and tumor microenvironment remodeling.
Results: Evidence supports a resistance ecosystem comprising resistant epithelial subclones, cancer-associated fibroblast/extracellular-matrix barriers, myeloid-rich suppressive niches, dysfunctional T cells, and immune-active tertiary lymphoid structure-like regions. scRNA-seq assigns resistance programs to specific cell states, whereas ST localizes these states to tumor-stromal interfaces, immune-excluded regions, and myeloid-rich foci.
Conclusion: These approaches complement one another in defining ovarian cancer resistance as a cellular and spatial ecosystem. Translation will require larger longitudinal cohorts, spatial multi-omics, and functional validation.
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