About

Yingzi Liu is an Assistant Professor of Radiation and Cellular Oncology at the Biological Sciences Division of the University of Chicago. She is also affiliated with the Committee on Medical Physics and is involved in graduate programs including Medical Physics and the PhD Program in Medical Physics. Her research focuses on the intersection of radiation and cellular oncology, contributing to the understanding and advancement of medical physics. She is actively engaged in academic and clinical initiatives within the University of Chicago Medicine and the Pritzker School of Medicine, supporting education and research in medical physics and related fields.

Research topics

• Composite material
• Materials science
• Nanotechnology
• Chemical engineering
• Optoelectronics
• Genetics
• Medicine
• Pharmacology
• Bioinformatics
• Biology
• Cancer research
• Computational biology

Selected publications

• DNA Methylation-Regulated FAM107A Affects Colorectal Carcinogenesis by Inhibiting FOXM1

  Journal of Investigative Surgery · 2026-03-18

  articleOpen access1st author

  INTRODUCTION: Family with sequence similarity 107 member A (FAM107A) has been reported to inhibit cancer cell proliferation and migration and enhance apoptosis; however, to our knowledge, the association between FAM107A and colorectal cancer (CRC) has not been explored. METHODS: CCK-8 assay, colony formation, EdU, flow cytometry assays were used to detect the cellular aggressive behaviors. FAM107A promoter methylation was analyzed by bioinformatics tools. The interaction between DNMT1 and FAM107A was explored by RT-qPCR, Western blot and ChIP assay. RESULTS: < .001). DISCUSSION: These results hypothesize that the occurrence and development of CRC are mainly mediated by the DNMT1/FAM107A/FOXM1 axis.

  PublisherDOI

• FAM107A inhibits Invasion and migration of colorectal cancer by affecting EMT via the AKT pathway.

  PubMed · 2025-12-09 · 1 citations

  articleSenior author

  Metastasis of colorectal cancer (CRC) is the main cause of CRC-related mortality. FAM107A is widely expressed in various normal tissues. However, few studies have revealed the biological function of FAM107A in epithelial-mesenchymal transition (EMT) in human cancer cells, and the related molecular mechanisms and signaling cascades are completely unknown. Here, we found that FAM107A was abnormally expressed in human CRC tissues and cell lines. Further research has shown that overexpression of FAM107A through transfection weakened the expression level of EMT-related markers. In addition, our research results indicated that upregulation of FAM107A inhibited the AKT signaling cascade in human CRC cells, while AKT activators restored activation of p50, indicating that FAM107A may regulate EMT through AKT activation of p50. Our results suggest that FAM107A could be a potential target for the treatment of CRC.

  PublisherDOI

• Adaptability and stress response mechanisms of abalone Haliotis discus hannai to cadmium in vitro and in vivo

  Aquaculture · 2025-09-30

  article1st author
  PublisherDOI

• Random mutagenesis and semi-rational design enhance the tolerance of Metabacillus litoralis C44 α-L-rhamnosidase

  International Journal of Biological Macromolecules · 2025-04-08

  article
  PublisherDOI

• Telomerase reverse transcriptase degradation via a rationally designed covalent proteolysis targeting chimera

  Bioorganic & Medicinal Chemistry Letters · 2025-05-22

  article
  PublisherDOI

• Non-canonical splice variant of PFKFB4 in hepatocellular carcinoma activates AKT through direct interaction

  JHEP Reports · 2025-08-26

  articleOpen access

  Background & Aims: The glycolytic enzyme 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 4 (PFKFB4) has emerged as a vital oncogene in many cancer types as a result of its metabolic function and signaling pathways. However, the effects of alternative splicing variants of PFKFB4 remain largely unexplored. Methods: kinase assays, and immunoprecipitation. Results: = 0.001). Conclusions: Our study highlights the oncogenic characteristics of the novel PFKFB4-ΔEx6 variant in HCC. The direct effect of PFKFB4-ΔEx6 on AKT activation underscores its role in HCC progression and as a therapeutic biomarker for mTOR/AKT inhibitors. Impact and implications: Our study identified a non-canonical variant of PFKFB4 as a crucial activator of the AKT/mTOR signaling pathway in HCC. This discovery reveals a novel oncogenic mechanism that extends beyond the conventional role of PFKFB4 in metabolism. The PFKFB4-ΔEx6 variant enhances tumor progression and renders HCC cells sensitive to everolimus, indicating its potential as both a prognostic biomarker and a therapeutic target. Given the clinical importance of mTOR/AKT inhibitors, PFKFB4-ΔEx6 could act as a predictive marker for treatment response, paving the way for personalized therapeutic strategies in HCC. These findings provide new insights into the functional diversity of glycolytic enzymes in cancer biology and targeted therapy.

  PublisherOA PDFDOI

• Abstract 4098: PARP1 and EZH2 independently limit 5'-3' end resection to promote rapid DNA repair after radiation

  Cancer Research · 2025-04-21

  article

  Abstract Cellular metabolism and epigenetic regulation have overlapping roles in cancer cell responses to radiation, with dynamic, reversible post-translational modifications including poly-ADP-ribosylation, O-GlcNAcylation and methylation emerging as key targets. This study explored crosstalk between poly-ADP-ribose polymerase 1 (PARP1), O-GlcNAc transferase (OGT), and the PRC2 subunit and histone methyltransferase EZH2 in the context of DNA double-strand break (DSB) repair. We focused on 5'-3' end resection, which determines repair pathway choice during S and G2 via guiding DSB repair away from non-homologous end joining (NHEJ) and toward homologous recombination (HR). DSB repair was examined in the human breast cancer cell line MCF7 using neutral comet assay and immunofluorescent detection of γH2AX, 53BP1, and BRCA1 foci. 5'-3' end resection was followed by tracking BrdU, RPA and RAD51 foci. We used CRISPR RNP to form pools of PARP1 and EZH2 knockout (KO) cells. After irradiation, both PARP1 KO and PARP inhibitor veliparib-treated cells displayed persistent DSBs and increased ssDNA, each restricted to S/G2 cells. While increased 5'-3' end resection may result from NHEJ defects, deregulation of resection may divert DSBs away from NHEJ to saturate cellular capacity for HR. Indeed, PARP inhibition enhanced HR repair based on a repair pathway reporter. Increasing protein O-GlcNAcylation in PARP1 KO or veliparib-inhibited cells restored DSB repair and suppressed hyper-resection, suggesting an independent, OGT-regulated determinant of pathway choice. Prior studies had implicated EZH2 and resulting histone H3 K27 trimethylation in promoting NHEJ and as a mediator of O-GlcNAcylation effects. Much like PARP1 KO, irradiated EZH2 KO cells displayed an S/G2 DSB repair defect associated with increased ssDNA. Hyper-resection in EZH2 KO was enhanced by PARP inhibition but modulating O-GlcNAcylation had no effect. Interestingly, along with increased nuclear BrdU foci, irradiated PARP1 KO and EZH2 KO each displayed cytosolic ssDNA foci. We infer that limiting NHEJ repair and/or promoting 5'-3' end resection in S/G2 can overwhelm HR, leading to hyper-resection, cytosolic DNA, and inflammation. Toward overcoming resistance to PARP inhibitors, O-GlcNac metabolism, OGT activity and its downstream mediator EZH2 offer attractive targets for therapeutic intervention. Overall, strategies aimed at deregulating 5'-3' end resection may help focus effects of genotoxic stress on proliferating cells and potentiate combinations with immunotherapies. Citation Format: Elena Efimova, Yue Liu, Sera Averbek, Isabelle Lomeli, SeokGyeong Choi, Sojung Ha, Woo-Young Kim, Stephen J. Kron. PARP1 and EZH2 independently limit 5'-3' end resection to promote rapid DNA repair after radiation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 4098.

  PublisherDOI

• Molecular mechanisms of acquired resistance to EGFR tyrosine kinase inhibitors in non-small cell lung cancer

  Drug Resistance Updates · 2025-06-09 · 20 citations

  review
  PublisherDOI

• Vacuum‐Evaporated Perovskite and Interfacial Modifier for Efficient Perovskite Solar Cells

  Small · 2025-05-02 · 4 citations

  article

  Abstract Surface passivation of the perovskite layer is crucial for enhancing the photovoltaic performance of perovskite solar cells (PSCs). Vacuum evaporation is a scalable solvent‐free method for depositing a uniform and homogenous thin layer with better control of film thickness. While the use of the vacuum‐deposition method to obtain high‐quality perovskite thin films is recently adapted, the evaporation of organic additives for surface passivation of the perovskite layer has not been widely studied. In this work, a vacuum evaporation method is introduced to uniformly deposit a novel multifunctional organic salt, 2‐chlorophenethylamine pentafluorobenzene sulfonate (2‐ClPEAPf), onto a perovskite surface. It is observed that 2‐ClPEAPf not only effectively passivates the interfacial defects but also prevents moisture invasion into the perovskite film. As a result, planar n–i–p PSCs exhibit maximum PCE up to 25.16% with an aperture area of 0.1 cm 2 and PCE of 24.00% (certified) on an active area of 1.0 cm 2 . In addition, the 0.1 cm 2 device with vacuum‐evaporated 2‐ClPEAPf reveals enhanced operational stability maintaining 92.5% of its initial efficiency after 800 hours of continuous light irradiation.

  PublisherDOI

• Tumor targeting dendritic nanocarrier with immunogenic cell death inducing and TIGIT blockade for synergistic chemo-immunotherapy against TNBC

  Journal of Nanobiotechnology · 2025-12-07

  articleOpen access

  The clinical therapeutic effect of immune-checkpoint blockade (ICB) on triple-negative breast cancer (TNBC) is limited due to low tumor immunogenicity and tumor immunosuppressive microenvironment. Combination therapies of chemotherapy and ICB have been confirmed efficacious. Herein, poly(L-lysine) dendrimer (PLLD) nanosphere (PR-T@PLLD) integrating chemotherapeutic drug paclitaxel (PTX), natural anti-tumor compound Rubioncolin C (RC) and TIGIT/PVR blocking peptide DTBP-3 is constructed for chemo-immunotherapy of anti-PD-1 resistant tumor. The PEGylation and DTBP-3 modification endow PR-T@PLLD with prolonged blood circulation, enhanced tumor penetration and improved internalization. In the acidic environment of lysosomes, PR-T@PLLD disassembles and releases PTX, RC and DTBP-PLLD. The cell death induced by PTX is significantly enhanced through synergy with RC. RC collaborated PTX also triggers robust immunogenic cell death that efficiently increases tumor infiltration of cytotoxic T lymphocytes (CTLs). Additionally, the released DTBP-PLLD inhibits the exhaustion of CTLs via directly binding to TIGIT and blocking the interaction of TIGIT with its ligand PVR. Thus, PR-T@PLLD arouses a conspicuous anti-tumor immune response via increasing income and reducing expenditure of CTLs. Moreover, PR-T@PLLD reduces the recruitment of immunosuppressive cells in tumor. PR-T@PLLD also inhibits tumor metastasis through evoking immune memory response and inhibiting epithelial-mesenchymal transition and extracellular matrix degradation. In general, PR-T@PLLD is a promising nanoplatform realizing synergistic enhancement of chemo-immunotherapy against anti-PD-1 resistant TNBC.

  PublisherDOI

Frequent coauthors

• Stephen J. Kron

  University of Chicago

  34 shared

• Donald J. Wolfgeher

  University of Chicago

  21 shared

• Elena V. Efimova

  21 shared

• Aishwarya Ramamurthy

  19 shared

• Vytautas P. Bindokas

  17 shared

• Natalia Ricco

  17 shared

• Amy C. Flor

  17 shared

• Oliver K. Appelbe

  17 shared

Labs

• Yingzi Liu's LabPI

  1-2 sentence research focus