Cancer Mechanics
Mechanical properties of cancer cells.
Viscoelasticity · creep · cellular mechanics · cytoskeleton · heterogeneity · breast cancer · triple-negative breast cancer
Research archive
Years spent investigating how disease changes biology at the cellular, mechanical, and material levels.
Research
Mechanical properties of cancer cells.
Viscoelasticity · creep · cellular mechanics · cytoskeleton · heterogeneity · breast cancer · triple-negative breast cancer
Single-cell mechanics in normal and neoplastic brain cells.
Glioblastoma · single-cell mechanics · viscoelastic properties · brain microenvironment · brain metastasis
How physical and metabolic conditions shape disease behavior.
Mechanical stress · immune escape · mechanical/metabolic interactions · tumor microenvironment
Engineering materials for targeted delivery and treatment.
Magnetite nanoparticles · PDMS · PLGA/PCL · doxorubicin · hyperthermia · photothermal treatment
Research story / 01
The question. Can cancer cells be distinguished through their mechanical behavior?
The approach. Single-cell mechanical characterization, viscoelastic creep analysis, cytoskeletal characterization, and quantitative/statistical analysis.
The finding. Investigated measurable differences and heterogeneity in malignant and non-malignant cell behavior.
Why it matters. The work provides a scientific framework for exploring mechanical properties as potential biomarkers for cancer detection.
Research story / 02
The question. How do normal and neoplastic brain cells compare mechanically at the single-cell level?
The approach. A single-cell mechanical assay and analysis of viscoelastic behavior in normal brain cells and glioblastoma cells.
The finding. The 2024 Biophysical Journal work produced a nuanced comparison rather than forcing a simplistic “cancer is softer or harder” narrative.
Why it matters. Mechanical behavior is heterogeneous and context-dependent, which makes careful measurement essential to meaningful interpretation.
Selected publications include work in Biophysical Journal, Journal of Functional Biomaterials, Journal of Materials Science: Materials in Medicine, Cells, Frontiers in Oncology, and Journal of Biomedical Materials Research.
Published research
Peer-reviewed work connecting scientific curiosity to a body of evidence — each with the finding, why it matters for innovative medicine and therapies, and the full paper to download.
10
Peer-reviewed publications
9
Scientific journals
2022–2026
Years of active research
100%
Full text downloadable
Featured work

Nwazojie, Obayemi, Salifu, Borbor-Sawyer, Uzonwanne, Onyekanne, Akpan, Onwudiwe, Oparah, Odusanya, Soboyejo
The finding. EphA2-targeted prodigiosin and paclitaxel encapsulated in PLGA-PCL microspheres sustained drug release for 90–140 days, killed triple-negative breast cancer cells in vitro, and eliminated residual tumors in mice after surgical resection — with no metastasis or organ toxicity 12 weeks later. Non-targeted drug formulations, by contrast, allowed the tumors to regrow.
Why it matters. This is a blueprint for an implantable, tumor-bed-specific drug depot: place it where a tumor was just removed and let it release a targeted drug on its own schedule. That kind of localized, receptor-targeted, sustained release is exactly what is needed to cut systemic chemotherapy toxicity while directly attacking the cells most likely to cause recurrence.

The finding. Using a microfluidic shear assay and digital image correlation, glioblastoma cells and normal astrocytes showed statistically indistinguishable stiffness, viscosity, and stress-relaxation behavior — unlike breast, bone, and kidney cancers, where malignant cells are consistently softer than their normal counterparts.
Why it matters. This result is a caution against a one-size-fits-all "cancer cells are softer" biomarker and points to why glioblastoma so rarely spreads outside the brain. It reframes where mechanical biomarkers and cell-mechanotyping diagnostics will and will not work, and it is a needed data point for anyone designing brain-specific liquid-biopsy or single-cell diagnostic tools.

The finding. Functional principal component analysis (fPCA) of single-cell creep-compliance time series — no manual model-fitting required — separated non-tumorigenic, less-metastatic, and highly-metastatic breast cells into distinguishable clusters. A single component (PC1), capturing overall creep compliance, explained over 98% of the variance and correlated strongly with independently measured cell modulus (-83%) and viscosity (-85%).
Why it matters. This replaces subjective, model-selection-dependent viscoelastic curve-fitting with an unbiased, automatable, data-driven pipeline for turning raw single-cell mechanical measurements into a cancer-malignancy signal — a step toward scalable, less-operator-dependent mechanical diagnostics and microfluidic screening tools.

The finding. This perspective synthesizes evidence that fluid shear stress and solid stress inside tumors activate epithelial–mesenchymal transition (EMT) and autophagy — two mechanisms cancer cells already use to resist T-cell and NK-cell killing and blunt the response to checkpoint-blockade immunotherapy.
Why it matters. It builds the case for combining mechanics-targeting drugs — anti-fibrotics, FAK/YAP inhibitors, angiotensin blockers — with immunotherapy, a rationale now being tested in real trials (losartan + nivolumab; pirfenidone + atezolizumab). It positions tumor mechanobiology as a new lever for improving immunotherapy response rates.

PDMS/magnetite nanocomposites with 1–10 wt.% reinforcement showed tunable stiffness and toughness that closely matched published breast-tissue moduli, validated against composite and crack-toughening models (crack deflection and bridging), while gaining thermal stability from the magnetite filler.

This perspective maps how the brain’s glucose abundance, softer extracellular matrix, and YAP/TAZ mechanotransduction jointly reprogram the metabolism (glycolysis, lipid and cholesterol synthesis) and mechanics (cell stiffening) of breast cancer cells once they colonize the brain.

Shear-assay creep mapping of individual cells showed triple-negative breast cancer cells have measurably lower actin and keratin-18 density, higher creep rates, and lower stiffness/viscosity than normal breast cells — with creep strain following a lognormal distribution and viscoelastic properties following normal distributions.

Near-infrared laser exposure of magnetite/PDMS nanocomposites reached hyperthermic temperatures (41–44°C), reduced triple-negative breast cancer cell viability in vitro, and heated safely through chicken tissue without physical damage — with a finite-element heat-transport model matching the experimental temperature and thermal-dose results.

Dextran-capped MCM-41 silica nanoparticles gave sustained release of doxorubicin over 30 days; the AMACR-antibody-targeted formulation outperformed free doxorubicin at inhibiting prostate cancer cell growth over 96 hours, with full release kinetics and thermodynamics characterized.

LHRH-conjugated prodigiosin and paclitaxel released from magnetite-modified PDMS devices over 30 days at 37–44°C produced significantly higher triple-negative breast cancer growth inhibition than unconjugated drugs, with flow cytometry confirming induction of early- and late-stage apoptosis.