Triple-negative breast cancer (TNBC) remains one of the most therapeutically resistant breast cancers and often displays pronounced immune heterogeneity. This study integrates multi-omics datasets to identify candidate biomarkers that may influence TNBC progression and modulate therapeutic response.
Transcriptomic, DNA methylation, microRNA (miRNA), and single nucleotide polymorphism (SNP) datasets from public repositories were analyzed using differential expression and correlation pipelines. Expression, mutation, and regulatory metrics were then integrated to prioritize key genes. Top candidates, including CCND2 and KIF1A, were preliminarily validated using qPCR and Kaplan—Meier plots. CIBERSORT was applied to examine tumor immune cell infiltration and to assess the immune-related expression of candidate genes.
Multi-omics integration highlighted CCND2 and KIF1A as highly ranked candidates associated with TNBC proliferation and cell cycle regulation. Literature and pathway analysis suggested potential involvement of these genes in key oncogenic and immune-related signaling pathways. Preliminary qPCR results supported their differential expression relative to normal breast tissue.
These findings nominate CCND2 and KIF1A as candidate biomarkers and potential therapeutic targets in TNBC. Continued pathway and functional validation will clarify how these genes contribute to tumor progression and may inform precision treatment strategies for TNBC.
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Translational and Interventional Immunology (TI)
Roberto Aguilar, Victor Wang, Shane Deng· Journal of Immunology· 0 citations
Melanoma progression is driven by transcriptional and cytoskeletal regulators that influence cell proliferation, migration, and immune evasion. ZFC3H1, a zinc finger RNA-binding protein involved in nuclear RNA decay, and DYNLT3, a dynein light-chain component implicated in intracellular transport and signaling, are both aberrantly expressed in melanoma according to public transcriptomic datasets. This study investigates the functional roles of ZFC3H1 and DYNLT3 in A375 melanoma cells to determine whether their dysregulation contributes to tumor growth or survival.
Differential expression analysis of RNA-seq data from melanoma and normal skin samples identified ZFC3H1 and DYNLT3 as upregulated genes. CRISPR-Cas9 knockouts were generated in A375 cells to assess loss-of-function effects. RNA extraction and cDNA synthesis confirmed knockout efficiency by qPCR. Cell viability and proliferation were evaluated using trypan blue exclusion and standard colorimetric assays. Ongoing assays are examining changes in morphology and expression of stress-response genes following knockout.
Preliminary results confirmed robust expression of ZFC3H1 and DYNLT3 in wild-type A375 cells and successful CRISPR knockout in target lines. Early viability assays suggest reduced proliferation in DYNLT3-deficient cells, while ZFC3H1 knockout shows altered morphology consistent with cytoskeletal disruption. Additional analyses are underway to quantify transcriptional and phenotypic effects relative to control cells.
Loss-of-function analysis of ZFC3H1 and DYNLT3 in A375 melanoma cells provides new insight into their potential roles in tumor cell growth and regulation. These findings may help define RNA-processing and transport mechanisms that support melanoma progression and identify novel targets for therapeutic intervention.
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Tumor Immunology: Cellular Responses and Tumor Microevironment (TIME)
Roberto Aguilar, Aanvee Chawda, Elle Swoope· Journal of Immunology· 0 citations