Li Lan
· Associate Professor of Molecular Genetics and MicrobiologyDuke University · Microbiology and Immunology
Active 1999–2025
About
Li Lan is an Associate Professor of Molecular Genetics and Microbiology, as well as in Pharmacology and Cancer Biology, and a member of the Duke Cancer Institute. Her lab is dedicated to researching how cancer cells respond to DNA damage through DNA repair mechanisms and developing innovative strategies to target these pathways in cancer therapy. Her significant contributions include uncovering the critical role of PARP in DNA repair, leading to successful applications of PARP inhibitors in the treatment of breast, ovarian, and other types of cancer. Her research studies how DNA responds to oxidative damage at specific chromosomal locations, advancing understanding of DNA damage response in different chromosomal environments. Recently, her investigations have revealed a novel mRNA and R-loop-dependent DNA repair pathway that acts as a protective mechanism for transcribed regions of the genome, introducing a new paradigm in DNA repair research. Her research interests encompass unraveling the mechanisms of mRNA and R-loop-dependent DNA repair (RDDR) in cancer, developing targeted therapies, and exploring the molecular regulation of the RDDR pathway, including its interaction with DNA replication and chromatin remodeling. She employs screening platforms to monitor RDDR and aims to develop inhibitors that disrupt RDDR in cancer cells, as well as identify biomarkers for patient stratification and therapy response prediction. Her work also explores the potential applications of RDDR in gene editing and investigates the response of telomeres to oxidative damage in cancer, aiming to exploit vulnerabilities in cancer cells. Additionally, her research explores the interplay between DNA damage response and immune response in cancer, particularly the role of the DNA sensor cGAS in modulating the tumor microenvironment to enhance anti-tumor immunity. Overall, her lab strives to advance understanding of DNA repair processes in cancer and translate these findings into innovative therapeutic strategies to improve patient outcomes.
Research topics
- Biology
- Cell biology
- Genetics
- Molecular biology
Selected publications
Brain Research Bulletin · 2025-03-26 · 2 citations
articleOpen accessEvidence suggests that cognitive impairments due to obstructive sleep apnea (OSA) are related to abnormal lipid metabolism. Abnormal lipid metabolism in the brain might be a potential cause of neurodegeneration. Nonetheless, there is limited clarity regarding the comprehensive lipid metabolism changes in the hippocampus induced by chronic intermittent hypoxia (CIH). Targeted lipidomic analysis of mouse hippocampus and HT22 cells was essential to exploring changes in lipid metabolism after CIH exposure. The approach was used to quantify 575 lipid species in mouse hippocampus and 1285 lipid species in HT22 cells, belonging to 6 different classes. Among those lipid classes, glycerophospholipids (GP), fatty acyls (FA), sphingolipids (SP), glycerolipid (GL), and prenol lipids (PR) were not significantly changed in mouse hippocampus under CIH conditions, but steroid (ST) levels were significantly reduced. Based on in vitro results, CIH exposure significantly raises the levels of several lipids, including GP, PR, SP, and ST. However, GL and FA did not change significantly. Notably, in vivo as well as in vitro experiments showed down-regulation of LPI (16:0), LPI (18:0), PC (18:1/20:4), PE (O-18:0/16:0), PE (O-16:0/22:6), PI (18:0/18:0), and up-regulation of PI (18:0/19:2). Additionally, in CIH conditions, lipid droplets (LDs) typically accumulate as a result of metabolism disorders. Disorders of lipid metabolism and the abnormal accumulation of LDs in neurons cause neuronal damage and behavioral disorders. The altered levels of LPI, PC, PE, and PI in OSA patients might provide new insights into understanding lipid metabolism disorders in the nervous system.
Asian Journal of Surgery · 2025-11-20
articleOpen access1st authorTranslational Oncology · 2025-12-06 · 1 citations
articleOpen accessCircular RNAs (circRNAs), a class of covalently closed noncoding RNAs with remarkable stability and cell-type specificity, have emerged as critical regulators of cancer immunology. Increasing evidence reveals that circRNAs orchestrate tumor immune escape through multilayered mechanisms spanning post-transcriptional, post-translational, and metabolic levels, thereby reshaping the tumor immune microenvironment (TIME). A central theme involves the maintenance of PD-L1 homeostasis: circRNAs modulate PD-L1 stability via m^6A/IGF2BP-dependent RNA-protein interactions, protect PD-L1 from ubiquitin-mediated degradation through deubiquitinases, or promote its phosphorylation to prevent proteasomal turnover. Beyond tumor-intrinsic regulation, circRNAs are packaged into exosomes or small extracellular vesicles and delivered to immune cells, where they induce CD8^+ T-cell dysfunction, foster regulatory T-cell expansion, or reprogram myeloid-derived suppressor cells and macrophages toward immunosuppressive phenotypes. These intercellular communications contribute to resistance against immune checkpoint inhibitors and conventional therapies. In parallel, circRNAs are increasingly recognized as both therapeutic targets and agents. Strategies that silence oncogenic circRNAs using nanoparticles restore drug sensitivity and reinvigorate antitumor immunity, while synthetic or in vitro-transcribed circRNAs encoding immunostimulatory factors such as IL-12 demonstrate potent capacity to remodel TIME. The integration of tumor-tailored lipid nanoparticles, biomimetic vesicles, and rational circRNA design underscores a new wave of precision immunotherapy. This review highlights the mechanistic diversity of circRNAs in immune evasion, their roles in therapeutic resistance, and the translational opportunities offered by nanomedicine-based delivery systems. By bridging basic immunology and therapeutic innovation, circRNAs hold promise as next-generation targets and tools in cancer immunotherapy.
Nature Communications · 2025-01-29 · 27 citations
articleOpen accessFerroptosis is a form of iron-dependent programmed cell death, which is distinct from apoptosis, necrosis, and autophagy. Mitochondria play a critical role in initiating and amplifying ferroptosis in cancer cells. Voltage-Dependent Anion Channel 1 (VDAC1) embedded in the mitochondrial outer membrane, exerts roles in regulation of ferroptosis. However, the mechanisms of VDAC1 oligomerization in regulating ferroptosis are not well elucidated. Here, we identify that a VDAC1 binding protein V-Set and Transmembrane Domain Containing 2 Like (VSTM2L), mainly localized to mitochondria, is positively associated with prostate cancer (PCa) progression, and a key regulator of ferroptosis. Moreover, VSTM2L knockdown in PCa cells enhances the sensitivity of RSL3-induced ferroptosis. Mechanistically, VSTM2L forms complex with VDAC1 and hexokinase 2 (HK2), enhancing their binding affinity and preventing VDAC1 oligomerization, thereby inhibiting ferroptosis and maintaining mitochondria homeostasis in vitro and in vivo. Collectively, our findings reveal a pivotal role for mitochondria-localized VSTM2L in driving ferroptosis resistance and highlight its potential as a ferroptosis-inducing therapeutic target for the treatment of PCa.
Cell Death and Differentiation · 2025-12-17
articleSenior authorCancer Research · 2025-03-11
article1st authorCorrespondingAbstract The RNA methyltransferase TRDMT1 generates 5-methyl Cytosine (m5C) at R-loops which promotes transcription coupled homologous recombination (TC-HR) and thus impedes cellular sensitivity to R-loop induced DNA double-strand breaks (DSBs) at transcribing regions of the genome. We performed TRDMT1 inhibitor based drug screening approach in 300 cancer cell lines and identifies key factors associated with DNA mismatch repair (MMR) pathway especially in solid tumors. The R-loop accumulation correlated to severe replication stress and generated more transcription replication conflicts (TRCs) in TRDMT1 and MMR deficient background. Our study revealed synthetic lethal interactions between TRDMT1 and MMR which can provide a promising future strategy for improving treatment of solid tumors. Citation Format: Li Lan. Exploring the synthetic lethal interactions between mRNA methyl-5-cytocine at sites of R-loops and mismatch repair deficiency in solid tumor [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Functional and Genomic Precision Medicine in Cancer: Different Perspectives, Common Goals; 2025 Mar 11-13; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2025;85(5 Suppl):Abstract nr B010.
Biosensors and Bioelectronics · 2025-01-21 · 17 citations
articleResearch on Application of Gesture Interaction Technology Based on Computer Vision
2025-04-25
articleSenior authorThe application of gesture recognition technology based on computer vision in the field of human-computer interaction is analyzed. A hierarchical design idea of gesture interaction system based on computer vision is proposed. A new idea for judging the bending state of the finger is provided, and the bending state of the finger is used as a gesture feature to realize gesture classification, the application example vividly show that application field of gesture interaction. It is verified that the gesture interaction technology based on computer vision has the advantages of low hardware requirements, and natural and intuitive interaction experience. In order to expand the application scenario of gesture interaction technology.
Baseline Blood Oxygen Saturation Test Method and Test Results
Lecture notes in electrical engineering · 2025-10-22
book-chapterSenior authorFrontiers in Medicine · 2025-01-24 · 2 citations
articleOpen accessBackground Pralsetinib is a selective RET inhibitor. The ARROW trial revealed that RET fusion-positive non-small-cell lung cancer (NSCLC) can benefit from pralsetinib with tolerable adverse events (AEs). However, the efficacy and safety of pralsetinib in real world has rarely been reported. Materials and methods This study reviewed the efficacy and safety of pralsetinib in RET fusion-positive NSCLC patients between March 2021 and December 2021. Progression-free survival (PFS) and overall survival (OS) were evaluated by a Kaplan-Meier analysis and log-rank test. A Cox regression model was performed to identify independent prognostic factors. Results A total of 28 patients were enrolled, and the median follow-up time was 18.1 months. The objective response rate and disease control rate of the whole cohort were 57.2% and 71.4%, respectively, and the median PFS and OS were 8.1 months [95% confidence interval (CI), 3.1–13.2] and 13.8 months (95% CI, 2.8–24.8), respectively. Baseline characteristics of the treatment naive group and pre-treated group were listed. The median PFS tended to be better in treatment naive group (18.3 vs. 8.0 months, P = 0.067), while the median OS were similar between the two groups (28.4 vs. 11.6 months, P = 0.308). Patients with Eastern Cooperative Oncology Group Performance Status (ECOG PS) score of 2 had worse median PFS comparing with those with ECOG PS score of 0–1 (3.8 vs. 12.6 months, P = 0.004). Besides, patients previously treated with platinum-based chemotherapy (PBC) also revealed worse median PFS comparing with those without previous PBC (8.0 vs. 18.6 months, P = 0.023). Furthermore, patients previously treated with anti-programmed death-1 (PD-1) antibody or multikinase inhibitors (MKIs) showed worse median OS compared with those without previous anti-PD-1 antibody (5.0 vs. 22.0 months, P = 0.002) or MKIs (6.2 vs. 28.4 months, P = 0.015). The most common AEs was increased aspartate aminotransferase (39.3%). Conclusion Pralsetinib was effective in RET fusion-positive NSCLC with tolerable AEs in real-world practice. Efficacy of pralsetinib was decreased in patients previously treated with PBC, immunotherapy, or MKIs.
Recent grants
NIH · $422k · 2016
NIH · $1.6M · 2022
Frequent coauthors
- 75 shared
Lee Zou
Harvard University
- 62 shared
Satoshi Nakajima
- 51 shared
Arthur S. Levine
University of Miami
- 46 shared
Yaqun Teng
Peking Union Medical College Hospital
- 39 shared
Akira Yasui
SPring-8
- 38 shared
Jian Ouyang
MUSC Hollings Cancer Center
- 38 shared
Haibo Yang
Shenyang University of Technology
- 38 shared
Leizhen Wei
Labs
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