Ke Liu

University of Florida

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Lijing Fang

Shenzhen Institutes of Advanced Technology

Huashun Li

Anhui University of Science and Technology

Hongchang Li

Shenzhen Institutes of Advanced Technology

Rui Wang

Lanzhou University

Lijiao Ao

Jinan University

Juntao Chen

First Affiliated Hospital of Henan University

Ximing Shao

Shenzhen Institutes of Advanced Technology

Chunlei Wu

State Key Laboratory of ASIC and System

Jianchao Zhang

First Affiliated Hospital of Zhengzhou University

Wu Su

Panyu Hospital of Chinese Medicine

Cooperative Institutions

Chinese Academy of Sciences

University of Florida

Zhengzhou University

Shandong University

Huazhong University of Science and Technology

Fudan University

Nanchang University

National Institutes of Health

Shandong First Medical University

Chinese Academy of Medical Sciences & Peking Union Medical College

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U.S. Food and Drug Administration Approval: Vismodegib for Recurrent, Locally Advanced, or Metastatic Basal Cell Carcinoma

Clinical Cancer Research (2013)

Michael D. Axelson Ke Liu Xiaoping Jiang Kun He Jian Wang

The data and regulatory considerations leading to the U.S. Food and Drug Administration (FDA) January 30, 2012 approval of Erivedge (vismodegib) capsules for the treatment of patients with recurrent, locally advanced, or metastatic basal cell carcinoma (BCC) are described. The FDA's approval decision was based primarily on the results observed in a single-arm, parallel cohort, international trial of vismodegib, administered orally at 150 mg daily until disease progression, in patients with pathologically confirmed, recurrent, locally advanced basal cell carcinoma (laBCC) or metastatic basal cell carcinoma (mBCC). An independent review committee confirmed an overall response rate (ORR) of 30.3% [95% confidence interval (CI): 15.6-48.2] in 33 patients with mBCC and an ORR of 42.9% (95% CI: 30.5-56.0) in 63 patients with laBCC; median response durations were 7.6 months and 7.6 months for patients with mBCC and laBCC, respectively. The most common adverse reactions were muscle spasms, alopecia, dysgeusia, weight loss, fatigue, nausea, diarrhea, decreased appetite, constipation, cough, arthralgias, vomiting, headache, ageusia, insomnia, and upper respiratory tract infection. Animal toxicology studies confirmed that vismodegib is a potent teratogenic agent. Approval was based on durable objective tumor responses supported by knowledge of the pathologic role of Hedgehog signaling in BCC and acceptable toxicity in a population without effective alternative therapies.

Vismodegib

10.1158/1078-0432.ccr-12-1956

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Figure S4 Cellular uptake and nuclear localization of PIPs. from Targeting Polo-like Kinase 1 by a Novel Pyrrole-Imidazole Polyamide–Hoechst Conjugate Suppresses Tumor Growth In Vivo

Ke Liu Lijing Fang Haiyan Sun Zhengyin Pan Jianchao Zhang

Hela cells or A549 cells stably expressing histone H2B-RFP were incubated with 10 μM of different PIPs for 24 h. Cells were then subjected to live-imaging using confocal microscopy. Scale bar, 10 μm.

HeLa

Conjugate

10.1158/1535-7163.22504989

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Supplementary Materials from Targeting Polo-like Kinase 1 by a Novel Pyrrole-Imidazole Polyamide–Hoechst Conjugate Suppresses Tumor Growth In Vivo

Ke Liu Lijing Fang Haiyan Sun Zhengyin Pan Jianchao Zhang

Supplementary Materials

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Imidazole

Pyrrole

10.1158/1535-7163.22504944.v1

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c-kit Is Required for Cardiomyocyte Terminal Differentiation

Circulation Research (2008)

Ming Li Nawazish Naqvi Eiji Yahiro Ke Liu Pamela C. Powell

c-kit, the transmembrane tyrosine kinase receptor for stem cell factor, is required for melanocyte and mast cell development, hematopoiesis, and differentiation of spermatogonial stem cells. We show here that in the heart, c-kit is expressed not only by cardiac stem cells but also by cardiomyocytes, commencing immediately after birth and terminating a few days later, coincident with the onset of cardiomyocyte terminal differentiation. To examine the function of c-kit in cardiomyocyte terminal differentiation, we used compound heterozygous mice carrying the W (null) and W(v) (dominant negative) mutations of c-kit. In vivo, adult W/W(v) cardiomyocytes are phenotypically indistinguishable from their wild-type counterparts. After acute pressure overload adult W/W(v) cardiomyocytes reenter the cell cycle and proliferate, leading to left ventricular growth; furthermore in transgenic mice with cardiomyocyte-restricted overexpression of the dominant negative W(v) mutant, pressure overload causes cardiomyocytes to reenter the cell cycle. In contrast, in wild-type mice left ventricular growth after pressure overload results mainly from cardiomyocyte hypertrophy. Importantly, W/W(v) mice with pressure overload-induced cardiomyocyte hyperplasia had improved left ventricular function and survival. In W/W(v) mice, c-kit dysfunction also resulted in an approximately 14-fold decrease (P<0.01) in the number of c-kit(+)/GATA4(+) cardiac progenitors. These findings identify novel functions for c-kit: promotion of cardiac stem cell differentiation and regulation of cardiomyocyte terminal differentiation.

Pressure overload

10.1161/circresaha.107.161737

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Design, synthesis and evaluation of halogenated phenazine antibacterial prodrugs targeting nitroreductase enzymes for activation

RSC Medicinal Chemistry (2023)

Ke Liu Tao Xiao Hongfen Yang Man‐Yun Chen Qiwen Gao

In this study, we have designed, synthesized, and evaluated new halogenated phenazine prodrugs that could lead to breakthroughs in the treatment of antibiotic-resistant bacterial infections.

Phenazine

Nitroreductase

10.1039/d3md00204g

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Copper-Mediated Direct Alkoxylation of Arenes Using an N,O-Bidentate Directing System

The Journal of Organic Chemistry (2014)

Lin‐Bao Zhang Xin‐Qi Hao Shou‐Kun Zhang Ke Liu Baozeng Ren

Highly effective CuCl-mediated C—H alkoxylation of arenes and heteroarenes has been developed by using a 2-aminopyridine 1-oxide moiety as an N,O-bidentate directing group. The reaction proceeds smoothly using a broad range of substrates to afford o-alkoxylated benzoic and heteroaromatic amide products. Moreover, the reaction system shows remarkable compatibility when hexafluoroisopropanol is used as a coupling parter; halogen, nitro, ether, alkoxy, ester, and sulfonyl functional groups are all tolerated. The directing group can be easily removed by base hydrolysis, affording o-alkoxylated benzoic acids.

Moiety

Amide

Benzoic acid

10.1021/jo502005j

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Design, Synthesis, and Evaluation of Carbonate-Linked Halogenated Phenazine-Quinone Prodrugs with Improved Water-Solubility and Potent Antibacterial Profiles

ACS Infectious Diseases (2023)

Tao Xiao Ke Liu Qiwen Gao Man‐Yun Chen Young S. Kim

Pathogenic bacteria have devastating impacts on human health as a result of acquired antibiotic resistance and innate tolerance. Every class of our current antibiotic arsenal was initially discovered as growth-inhibiting agents that target actively replicating (individual, free-floating) planktonic bacteria. Bacteria are notorious for utilizing a diversity of resistance mechanisms to overcome the action of conventional antibiotic therapies and forming surface-attached biofilm communities enriched in (non-replicating) persister cells. To address problems associated with pathogenic bacteria, our group is developing halogenated phenazine (HP) molecules that demonstrate potent antibacterial and biofilm-eradicating activities through a unique iron starvation mode of action. In this study, we designed, synthesized, and investigated a focused collection of carbonate-linked HP prodrugs bearing a quinone trigger to target the reductive cytoplasm of bacteria for bioactivation and subsequent HP release. The quinone moiety also contains a polyethylene glycol group, which dramatically enhances the water-solubility properties of the HP-quinone prodrugs reported herein. We found carbonate-linked HP-quinone prodrugs 11, 21–23 to demonstrate good linker stability, rapid release of the active HP warhead following dithiothreitol (reductive) treatment, and potent antibacterial activities against methicillin-resistant Staphylococcus aureus (MRSA), methicillin-resistant Staphylococcus epidermidis, and Enterococcus faecalis. In addition, HP-quinone prodrug 21 induced rapid iron starvation in MRSA and S. epidermidis biofilms, illustrating prodrug action within these surface-attached communities. Overall, we are highly encouraged by these findings and believe that HP prodrugs have the potential to address antibiotic resistant and tolerant bacterial infections.

Enterococcus faecalis

Pathogenic bacteria

Phenazine

10.1021/acsinfecdis.2c00558

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Role of LINC00240 on T-helper 9 differentiation in Allergic Rhinitis through influencing DNMT1-dependent methylation of PU.1

Authorea (Authorea) (2023)

Jianguo Liu Xunshuo Jiang Ke Liu Jianjian Deng Yi Qiu

Background Allergic rhinitis (AR) is a common allergic disease with increasing prevalence globally. However, the molecular mechanism underlying AR pathogenesis remains largely undefined. Methods Samples of peripheral blood and nasal mucosa from patients with AR, as well as the ovalbumin-induced AR mice model was obtained. qRT-PCR and western blot were used to detect the expression of LINC00240, miR-155-5p, PU.1 and other key molecules. ELISA assay and flow cytometry were employed to evaluate the secretion of IL-9 and T-helper 9 (Th9) cell ratio, respectively. Bioinformatics analysis, RNA immunoprecipitation (RIP), chromatin immunoprecipitation (ChIP) and luciferase reporter assays were employed to further elucidate the regulatory network of LINC00240/miR-155-5p/DNMT1. The methylation of PU.1 promoter was assessed by methylation-specific PCR (MSP). This signaling axis was finally confirmed in the AR mice model. Results LINC00240 was downregulated, while miR-155-5p and PU.1 were upregulated in the peripheral blood and nasal mucosa of AR patients, as well as in the AR mice. This was accompanied with the increased ratio of Th9 cells and elevated IL-9 secretion. Mechanistically, LINC00240 served as a miR-155-5p sponge, and DNMT1 was a target of miR-155-5p. In addition, DNMT1 mediated the methylation of PU.1 promoter. In vivo studies verified that LINC00240 mitigated AR progression, possibly via miR-155-5p/DNMT1/PU.1-dependent Th9 differentiation. Conclusion In summary, the involvement of LINC00240 in AR pathogenesis is closely associated with Th9 differentiation through modulating DNMT1-dependent methylation of PU.1 by sponging miR-155-5p.

DNMT1

Chromatin immunoprecipitation

Pathogenesis

10.22541/au.169366876.60294454/v1

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Supplementary Materials from Targeting Polo-like Kinase 1 by a Novel Pyrrole-Imidazole Polyamide–Hoechst Conjugate Suppresses Tumor Growth In Vivo

Ke Liu Lijing Fang Haiyan Sun Zhengyin Pan Jianchao Zhang

Supplementary Materials

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Imidazole

Pyrrole

10.1158/1535-7163.22504944

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Figure S5 Flow cytometry analysis of apoptosis upon PIP3 treatment. from Targeting Polo-like Kinase 1 by a Novel Pyrrole-Imidazole Polyamide–Hoechst Conjugate Suppresses Tumor Growth In Vivo

Ke Liu Lijing Fang Haiyan Sun Zhengyin Pan Jianchao Zhang

Hela cells were treated with or without 10 μM PIP3 for 72 hours and then labeled by Propidium iodide and Annexin V-FITC for detecting early and late apoptotic signal.

Propidium iodide

Conjugate

HeLa

10.1158/1535-7163.22504986

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