Epitranscriptomics & Multi-Omics Integration Analysis Services
Creative Biolabs provides a unified analytical environment designed to decode the "soft code" of cancer. We deliver actionable insights that allow researchers to identify "silent" drivers that single-omics approaches often miss. Our solutions facilitate the classification of research-relevant subtypes and the identification of metabolic hub proteins, providing a direct path to small-molecule inhibitor development. By integrating disparate data streams, we help your team move beyond static genomic snapshots toward a dynamic understanding of tumor plasticity.
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Introduction to Epitranscriptomics and Multi-Omics Integration
The advent of high-throughput profiling has revealed that cancer is a multilayered disorder where the "execution" of the tumor program is often post-transcriptional. Epitranscriptomics, particularly m6A RNA methylation, serves as the "missing link" between genomic blueprints and functional phenotypes. Recent literature underscores that co-regulation between DNA copy numbers and epigenetic modifications—such as promoter hypermethylation—dictates therapy resistance and tumor plasticity. Integrating these layers provides the only comprehensive view of the oncogenic program, essential for modern drug discovery, target validation, and identifying the molecular vulnerabilities of heterogeneous tumor cell populations.
Our Featured Services
Epitranscriptome Mapping & Analysis
Creative Biolabs provides high-resolution epitranscriptome mapping for m6A, m5C, and more. We decode "silent" drivers of tumor plasticity, offering precise biomarker identification and metabolic analysis to accelerate your small-molecule inhibitor development and cancer research.
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Regulatory Element-Gene Linking & Cistrome Integration
Creative Biolabs offers regulatory element-gene linking and cistrome integration to decode the cancer "regulome." We map enhancer-promoter interactions and transcription factor networks, identifying the master switches driving malignancy and therapeutic resistance.
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Multi-Omics Integration Analysis & Reporting
Creative Biolabs provides a unified multi-omics integration platform, decoding cancer's "soft code" by merging DNA methylation, RNA modifications, and chromatin accessibility. We identify silent drivers and metabolic hubs, offering actionable insights into tumor plasticity for precision therapeutic discovery.
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Key Deliverables and Solutions
At Creative Biolabs, we offer a modular and highly customizable multi-omics framework that scales from basic target screening to deep mechanistic validation. Our offerings are centered on the premise that epigenetic and epitranscriptomic modifications are the primary orchestrators of the cancer phenotype.
Epitranscriptomic Landscape Mapping
We provide high-resolution mapping of various RNA modifications beyond the standard transcriptome. Our platform utilizes MeRIP-Seq and miCLIP to pinpoint m6A, m5C, and pseudouridine sites, revealing how these modifications influence transcript stability and oncogenic translation.
Cross-Layer Co-Regulation Analysis
Our proprietary computational pipeline correlates DNA copy number variations with DNA promoter methylation and RNA-seq profiles. This integration identifies whether genes are silenced by physical loss or epigenetic braking, providing a multifaceted view of dysregulation.
Genome-Scale Metabolic Modeling
We offer specialized flux balance analysis integrating transcriptomic and metabolomic data to simulate cellular metabolism. This process identifies metabolic vulnerabilities and hub enzymes, such as squalene synthase, to disrupt energy production in drug-resistant tumor cells.
Immune Microenvironment Deconvolution
Using multi-omics signatures, we offer deep characterization of the immune landscape within models. We score Tumor-Infiltrating Lymphocytes and stromal involvement, helping researchers predict which subtypes are immune-hot or immune-cold to guide effective immunotherapy development.
AI-Driven Target Prioritization
Our platform utilizes machine learning algorithms, including random forest, to rank thousands of potential candidates. We focus on hub proteins with the highest connectivity across all omics layers to ensure your targets are biological masters.
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Workflow
Our integration process is engineered for scientific rigor and transparency, ensuring every data point is leveraged for maximum biological insight.
Publication
This review comprehensively explores the roles of epitranscriptomic (e.g., mRNA methylation, non-coding RNAs) and epiproteomic (post-translational) modifications in driving cancer drug resistance. It details how these regulatory layers alter drug response mechanisms and presents them as promising therapeutic targets. The article synthesizes evidence demonstrating that targeting specific "writer," "reader," and "eraser" proteins within these modification systems can potentially reverse resistance to chemotherapeutic agents like cisplatin, 5-fluorouracil, and EGFR-TKIs, offering novel strategies for cancer therapy.
Fig.1 Targeting epitranscriptomic and epiproteomic modifications to reverse chemoresistance. 1
Why Choose Us?
Creative Biolabs stands at the intersection of wet-lab excellence and advanced bioinformatics. Our pipeline is unique in its ability to map cross-layer co-regulation, ensuring that genomic instability—such as copy number variations (CNVs)—and epigenetic silencing are analyzed as synchronized events rather than isolated incidents. By integrating chromatin accessibility with structural variations, we capture the true complexity of oncogenic transformations. This holistic approach provides a competitive edge in identifying unique therapeutic windows that single-omic methods miss. Our platform bridges the gap between static DNA snapshots and the dynamic, multi-layered "soft code" driving tumor plasticity and drug resistance.
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FAQs
How does Creative Biolabs handle the integration of disparate data types like metabolomics and sequencing?
We employ advanced statistical frameworks such as joint non-negative matrix factorization and Bayesian networks. These methods ensure different data scales (e.g., discrete sequence counts vs. continuous mass spec peaks) are normalized and functionally correlated.
Can you perform this analysis on single-cell samples?
Yes, our pipeline includes ML-enabled annotation specifically designed for multilayered single-cell transcriptomic and epigenomic data, allowing for the characterization of rare cell populations.
Do you provide the identification of specific enzymes involved in m6A modifications?
Absolutely. Our reports identify the specific "writers" (e.g., METTL3), "erasers," and "readers" (e.g., YTHDF family) that are significantly dysregulated and driving your specific phenotype.
Customer Review
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Enhanced Subtype Discovery
Using Creative Biolabs' multi-omics in our research has significantly facilitated the identification of immune-desert clusters in our TNBC models, which were completely hidden in our previous single-layer RNA-seq data. The depth of their integrative reports provided a clear direction for our next project phase. – Dr. Al* S
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Validated Epitranscriptomic Drivers
The m6A-Seq integration allowed us to pinpoint the specific METTL3-driven pathway responsible for our compound's resistance. The network modeling provided by Creative Biolabs was exceptionally clear and bridged the gap between RNA methylation and metabolic output. – Prof. J* W
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How to Contact Creative Biolabs
Creative Biolabs provides a comprehensive analytical ecosystem that transforms complex biological data into actionable oncology research strategies. By mapping the interplay between the genome, epigenome, and metabolome, we empower researchers to overcome therapeutic resistance and accelerate the discovery of next-generation targets.
Contact Our Team for More Information and to Discuss Your Project
Reference
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Song, Huibin, et al. "Epitranscriptomics and epiproteomics in cancer drug resistance: therapeutic implications." Signal transduction and targeted therapy 5.1 (2020): 193. Distributed under Open Access license CC BY 4.0, without modification. https://doi.org/10.1038/s41392-020-00300-w
For Research Use Only | Not For Clinical Use
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