About
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Assistant Professor Adjunct
Biography
Dr. Mak's goal is to uncover the fundamental cell mechanics of cancer metastasis in order to provide insights towards novel anti-metastasis therapeutics. To achieve this, he is creating complementary experimental and computational platforms that can probe deeply into the multiscale mechanobiology of cancer cells. By exploring the biochemical and biomechanical signaling and feedback that regulate the mechanical state of cancer cells, such as their viscoelasticity and internal stresses, he will gain insights toward the factors and their mechanisms that lead to phenotypes that are conducive to invasive behavior. With his expertise in computational modeling of the mechanical properties of cells and developing experimental and microfluidic systems for studying cancer cell invasion dynamics, Dr. Mak seeks to overcome the hurdles of treating metastatic cancer.
Last Updated on March 06, 2025.
Departments & Organizations
Research
Overview
Medical Research Interests
Neoplasm Metastasis
ORCID
0000-0001-6881-8130
Research at a Glance
Yale Co-Authors
Frequent collaborators of Michael Mak's published research.
Publications Timeline
A big-picture view of Michael Mak's research output by year.
Barbara Ehrlich, PhD
Emma Kruglov
Stuart Campbell
Yibing Qyang, PhD
Christopher Anderson, BSc
Erica Herzog, MD, PhD
20Publications
150Citations
Publications
2025
Impact of Mechanical and Architectural Signals in the Tumor Microenvironment on Melanoma
Khan Z, Rossello‐Martinez A, Mak M. Impact of Mechanical and Architectural Signals in the Tumor Microenvironment on Melanoma. Advanced Healthcare Materials 2025, e01759. PMID: 40914820, DOI: 10.1002/adhm.202501759.Peer-Reviewed Original ResearchAltmetricConceptsDNA damageSolid mechanics simulationsPharmacological inhibition studiesSun-exposed melanomasActin polymerizationAcral melanomaHigh mechanical loadsTumor microenvironmentContractility inhibitorCollagen architectureCollagen hydrogelsCellular responsesDNADense tumor stromaMelanoma tumor microenvironmentMechanical loadingCellular morphologySingle cellsInhibition studiesLow sun exposureMechanical stressMechanical simulationsTherapeutic targetMicrofluidic platformMelanoma pathogenesisLZTR1 is a melanoma oncogene that promotes invasion and suppresses apoptosis
Bacchiocchi A, Mak M, Khan Z, Gong X, Sznol M, Na Z, Su H, Chan L, Yan Q, Zhao D, Mortlock R, Knight J, Slavoff S, Halaban R. LZTR1 is a melanoma oncogene that promotes invasion and suppresses apoptosis. Oncogene 2025, 44: 3974-3984. PMID: 40885854, PMCID: PMC12500468, DOI: 10.1038/s41388-025-03538-2.Peer-Reviewed Original ResearchAltmetricConceptsDegradation of ubiquitinated proteinsActin-related proteinsActin cytoskeleton organizationUbiquitin-proteasome systemSrc tyrosine kinaseAnchorage-independent growthNormal cell survivalCargo adapterActin organizationProximity biotinylationCytoskeleton organizationLC-MS/MS proteomicsLeucine zipperProteasome systemUbiquitinated proteinsCo-ImmunoprecipitationTargeting Pyk2Cell spreadingMelanoma cellsEnvironmental stressGrowth advantageMolecular characterizationCell migrationCell survivalLZTR1Monomethyl auristatin E and paclitaxel use different mechanisms to alter intracellular calcium signaling
Mendes G, Munshani S, Wachtler N, Wopfner H, Gong X, Sun Z, Mak M, Ehrlich B. Monomethyl auristatin E and paclitaxel use different mechanisms to alter intracellular calcium signaling. Biochemical Pharmacology 2025, 242: 117188. PMID: 40721011, PMCID: PMC12351507, DOI: 10.1016/j.bcp.2025.117188.Peer-Reviewed Original ResearchAltmetricConceptsMonomethyl auristatin EChemotherapy-induced peripheral neuropathyAntibody-drug conjugatesInositol trisphosphate receptorCalcium signalingCytotoxic agents to cancer cellsAuristatin ECalcium homeostasisAgents to cancer cellsPatients' qualityNCS-1Neurotoxic effectsIntracellular calcium levelsIntracellular calcium signalingPatients' quality of lifeTargeted cancer therapyMicrotubule-targeting agentsLithium co-treatmentPTX treatmentTrisphosphate receptorChemotherapy toleranceClinical successNeuronal calcium sensor-1Peripheral neuropathyCalcium levelsAdvanced tissue-engineered pulsatile conduit using human induced pluripotent stem cell-derived cardiomyocytes
Luo H, Anderson C, Li X, Lu Y, Hoareau M, Xing Q, Fooladi S, Liu Y, Xu Z, Park J, Fallon M, Thomas J, Gruber P, Elder R, Mak M, Riaz M, Campbell S, Qyang Y. Advanced tissue-engineered pulsatile conduit using human induced pluripotent stem cell-derived cardiomyocytes. Acta Biomaterialia 2025 PMID: 40582540, PMCID: PMC12338880, DOI: 10.1016/j.actbio.2025.06.055.Peer-Reviewed Original ResearchConceptsSingle ventricle congenital heart defectsHuman induced pluripotent stem cell-derived cardiomyocytesPluripotent stem cell-derived cardiomyocytesStem cell-derived cardiomyocytesCell-derived cardiomyocytesCongenital heart defectsHuman umbilical arteryUmbilical arteryHeart defectsPulmonary circulationDecellularized human umbilical arteriesHeart tissueLife-threatening defectsLife-threatening disorderLong-term complicationsEngineered Heart TissueFontan surgeryFunctioning ventriclePrompt treatmentHeart failureSpontaneous beatingPump functionImprove outcomesPressure generationConventional treatmentInstant assembly of collagen for tissue engineering and bioprinting
Gong X, Wen Z, Liang Z, Xiao H, Lee S, Rossello‐Martinez A, Xing Q, Wright T, Nguyen R, Mak M. Instant assembly of collagen for tissue engineering and bioprinting. Nature Materials 2025, 24: 1307-1318. PMID: 40481243, DOI: 10.1038/s41563-025-02241-7.Peer-Reviewed Original ResearchCitationsAltmetricConceptsCollagen bioinkElement methodBioprinting approachScaffold materialsTissue engineeringFabrication methodGelation kineticsCollagen constructsCells self-assembledUnmodified collagenBioprintingBiofabricationArchitectural cuesAssembly of collagenLiquid-gel transitionSelf-AssemblyRegenerative medicineEngineeringPH neutralizationBioinkMacro-andRapid assemblyCollagenous elementsAssemblyKineticsApplication of instant assembly of collagen to bioprint cardiac tissues
Xiao H, Liang Z, Gong X, Jordan S, Rossello-Martinez A, Gokhan I, Li X, Wen Z, Lee S, Campbell S, Qyang Y, Mak M. Application of instant assembly of collagen to bioprint cardiac tissues. APL Bioengineering 2025, 9: 026124. PMID: 40520649, PMCID: PMC12165719, DOI: 10.1063/5.0252746.Peer-Reviewed Original ResearchConceptsTissue engineeringFabrication of biomimetic tissuesCardiac tissue engineeringSupport bathCollagen bioinkBioprinting techniquesBiomimetic tissuesBioprinting methodsEngineered tissuesFabrication techniquesImmediate gelationBioprintingComplex tissue geometriesPolydimethylsiloxaneStructural fidelityNutrient diffusionFabricationTissue geometryEngineeringDamaged heart tissueBioinkStructural supportCardiac modelsCardiac tissueTissue maturationAdaptation to Volumetric Compression Drives an Apoptosis-Resistant and Invasive Phenotype in Liver Cancer.
Gong X, Ogino N, Leite M, Zhang D, Chen Z, Nguyen R, Liu R, Kruglov E, Flores K, Cabral A, Moreira de M Mendes G, Ehrlich B, Mak M. Adaptation to Volumetric Compression Drives an Apoptosis-Resistant and Invasive Phenotype in Liver Cancer. Cancer Research 2025, 85: 3156-3175. PMID: 40387600, PMCID: PMC12354003, DOI: 10.1158/0008-5472.can-24-0859.Peer-Reviewed Original ResearchCitationsAltmetricConceptsEpithelial-to-mesenchymal transition genesLiver cancerResistance to apoptosisCell state transitionsProliferation of tumor cellsYAP nuclear translocationCancer cell invasionIntracellular calcium signalingLiver cancer developmentTranscriptional dynamicsRac1 activationCellular protrusionsInhibiting Rac1Apoptosis-resistantTranscriptional changesInvasive phenotypeIntracellular calciumTumor cellsCell invasionNuclear translocationCancer developmentCalcium signalingTransition genesCancer cellsLiver-specific markersInvolvement of long non-coding RNA (lncRNA) MALAT1 in shear stress regulated adipocyte differentiation
Caron J, Ghanbariabdolmaleki M, Marino M, Qiu C, Wang B, Mak M, Wang S. Involvement of long non-coding RNA (lncRNA) MALAT1 in shear stress regulated adipocyte differentiation. Frontiers In Bioengineering And Biotechnology 2025, 13: 1570518. PMID: 40395673, PMCID: PMC12089105, DOI: 10.3389/fbioe.2025.1570518.Peer-Reviewed Original ResearchAltmetricConceptsShear stressMesenchymal stem cellsPhysiologically relevant shear stressRelevant shear stressAdipocyte differentiationDifferentiation of mesenchymal stem cellsInvolvement of long non-coding RNAsShearBiophysical cuesFluid shearLong non-coding RNAsMechanical microenvironmentDownregulation of MALAT1Mechanosensitive roleTargets of lncRNAsRegulates adipocyte differentiationLong noncoding RNAsNon-coding RNAsSilencing MALAT1Mechanical cuesLncRNA MALAT1Macromolecular crowding-based biofabrication utilizing unmodified extracellular matrix bioinks
Jordan S, Li X, Rossello-Martinez A, Liang Z, Gong X, Xiao H, Mak M. Macromolecular crowding-based biofabrication utilizing unmodified extracellular matrix bioinks. Acta Biomaterialia 2025, 198: 37-48. PMID: 40268621, PMCID: PMC12422595, DOI: 10.1016/j.actbio.2025.02.052.Peer-Reviewed Original ResearchMeSH Keywords and ConceptsConceptsDecellularized extracellular matrixExtrusion bioprintingComplex 3D structuresLayer-by-layer buildingCell scaffold materialsNatural extracellular matrixBiofabrication applicationsSolubilized extracellular matrixRobust hydrogelsLow printabilityTissue engineeringBioinkFabrication methodPromote biocompatibilityGelation timeBioactive scaffoldsPrintabilityBiofabricationNative tissueOrgan-specific extracellular matrixCrosslinkingExtracellular matrixBiocompatibilityExtrusionRegenerative medicine
2024
Viscosity regulates cell spreading and cell‐extracellular matrix interactions
Xiao H, Gong X, Jordan S, Liang Z, Mak M. Viscosity regulates cell spreading and cell‐extracellular matrix interactions. The FEBS Journal 2024, 292: 740-758. PMID: 39529371, PMCID: PMC12002552, DOI: 10.1111/febs.17306.Peer-Reviewed Original ResearchCitationsAltmetricConceptsCell spreadingRho-associated protein kinase 1Actin-related protein 2/3Regulation of cell locomotionRegulation of ECM remodelingCollagen substrateRas-related C3 botulinum toxin substrate 1Cell-extracellular matrix interactionsECM remodelingCellular remodelingExtracellular matrixEnhanced cell spreadingProtein kinase 1Membrane rufflingCell locomotionRemodeling of extracellular matrixCellular forcesSubstrate 1Cell migrationCellular spreadingKinase 1Matrix interactionsRac1MicrotubulesRegulation
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