A5101693447- Enzyme function and inhibition
- Click Chemistry and Applications
- Cholinesterase and Neurodegenerative Diseases
- Microtubule and mitosis dynamics
- Cellular Mechanics and Interactions
- Gut microbiota and health
- Genomics and Chromatin Dynamics
- Ubiquitin and proteasome pathways
- Colorectal Cancer Screening and Detection
- Bone health and osteoporosis research
- Cancer-related Molecular Pathways
- Phosphodiesterase function and regulation
- Cardiomyopathy and Myosin Studies
- Cell Adhesion Molecules Research
- 14-3-3 protein interactions
- Enhanced Recovery After Surgery
- Thyroid Cancer Diagnosis and Treatment
- DNA Repair Mechanisms
- Nuclear Structure and Function
- Salivary Gland Disorders and Functions
- Colorectal Cancer Surgical Treatments
- Bone health and treatments
- Bone Metabolism and Diseases
- Protist diversity and phylogeny
- Glutathione Transferases and Polymorphisms
University of California, Los Angeles
2020-2025
First Affiliated Hospital of Henan University of Science and Technology
2024
Sorrento Therapeutics (United States)
2023
First Affiliated Hospital of Harbin Medical University
2019-2022
Harbin Medical University
2015-2022
Columbia University
2001-2021
Kanazawa Medical University
2021
The First Affiliated Hospital, Sun Yat-sen University
2020
Zhongshan Hospital
2020
Fudan University
2020
Fusobacterium (F.) nucleatum is a carcinogenesis microbiota in colorectal cancer (CRC). Growing evidence shows that F. contributes to chemoresistance. Ferroptosis reported restore the susceptibility of resistant cells chemotherapy. However, role gut affecting ferroptosis chemoresistance remains unclear. Here, we examined CRC tissues patients using 16S rRNA sequencing investigate possible connection between dysbiosis and relapse CRC. We found high abundance tissue associated with relapse....
Bioengineered autologous cartilage-bone ramus-condyle grafts enable temporomandibular joint regeneration in a clinically sized porcine model.
Background Thyroid hormone withdrawal (THW) in postoperative thyroid cancer patients who need always accompanied by complications (e.g., dyslipidemia and constipation). At present, there are no effective safe means to alleviate these complications. Purpose We aimed assess the oral-gut microbiota profiles THW then investigate whether probiotics could alleviating related therapeutic effects were associated with state. Methods Fifty eligible carcinoma undergoing thyroidectomy randomly assigned...
A steady-state metaphase spindle maintains constant length, although the microtubules undergo intensive dynamics. Tubulin dimers are incorporated at plus ends of while they removed from minus ends, resulting in poleward movement. Such microtubule flux is regulated by rescue factors CLASPs kinetochores and depolymerizing protein Kif2a poles, along with other regulators How polymerization depolymerization coordinated remains unclear. Here we show that TPX2, a microtubule-bundling activator...
In the current assay, we applied green chemistry to synthesize silver nanoparticles (AgNPs) and incorporated curcumin-mediated AgNPs into polycaprolactone (PCL) nanofibers. The results showed that have a spherical morphology uniform shape with hydrodynamic diameter of around 112.9 nm polydispersity index 0.2. Moreover, zeta potential −3.7 mV. pristine PCL nanofibers 177 ± 37 PCL/AgNPs 163 34 nm. biological assessments (MTT Live/Dead assays) did not induce significant cell toxicity. disk...
KRAS is a potent oncogenic driver which results in downstream hyperactivation of MAPK signaling, while simultaneously increasing replication stress (RS) and accumulation DNA damage. KRASG12C mutations are common targetable alterations. Therapeutic inhibition eventual resistance to these inhibitors also known drive RS damage through adaptive mechanisms that maintain addiction high signaling. High levels result stronger reliance on cell cycle checkpoints, thereby introducing vulnerability...
Protein phosphatases are critical for regulating cell signaling, cycle, and fate decisions, their dysregulation leads to an array of human diseases like cancer. The dual specificity (DUSPs) have emerged as important factors driving tumorigenesis cancer therapy resistance. DUSP12 is a poorly characterized atypical DUSP widely conserved throughout evolution. Although no direct substrate has been firmly established, that implicated in protecting cells from stress, ribosomal biogenesis,...
<p>Combination of azenosertib With KRASG12C inhibitors in vivo increases median survival NSCLC models sensitive to inhibition</p>
<p>Combination of azenosertib with KRASG12C inhibitors improves efficacy and drives tumor regression in models CRC PDAC</p>
<p>Combination of azenosertib with <i>KRAS</i><sup>G12C</sup> inhibitors reduces tumor cell growth and induces DNA damage apoptosis <i>in vitro</i> in 3D. <b>A,</b> Seven-day combination treatment dose matrices NSCLC lines cultured as 3D spheroids. Cell viability was measured by CellTiter-Glo analyzed using the SynergyFinder tool. The Loewe additivity model is depicted which scores ≥10 are synergistic. Doses expressed μmol/L. arranged...
<p>Combination of azenosertib and KRASG12C inhibitors demonstrates synergy in NSCLC 2D vitro cellular assays by Bliss Independence model.</p>
<p>Combination of azenosertib and KRASG12C inhibitors or WEE1 knockdown demonstrates synergy in CRC, PDAC, NSCLC 2D cellular assays</p>
<p>Treatment of an NSCLC model with azenosertib + adagrasib results in biomarker changes vitro and vivo.</p>
<p>Treatment of an NSCLC CDX model with azenosertib + sotorasib results in tumor regressions and increased DNA damage apoptosis <i>in vivo</i>. <b>A,</b> Mean volume ± SEM subcutaneous NCI-H2122 xenografts NOD/SCID mice treated for 25 days (<i>n</i> = 9/group). <i>P</i> < 0.0001 all comparisons vehicle; combination compared monotherapies. <b>B,</b> Percent change (ΔTV) individual on day treatment. Values below 0 indicate...
<p>Combination of azenosertib with <i>KRAS</i><sup>G12C</sup> inhibitors shows efficacy in models innate and acquired resistance to G12C <i>in vivo</i>. <b>A,</b> Mean tumor volume ± SEM subcutaneous SW1573 xenografts NOD/SCID mice (<i>n</i> = 9/group). <b>B,</b> CR2528 PDX BALB/c nude treated for 24 days 8/group). <b>C,</b> NCI-H2030-R Xenografts were passaged grown maintained on 100 mg/kg sotorasib...
<p>Supplementary Data Figure Legends</p>
<p>Combination of azenosertib with <i>KRAS</i><sup>G12C</sup> inhibitors <i>in vivo</i> increases the depth and duration TGI in NSCLC models sensitive to inhibition. <b>A,</b> Mean tumor volume ± SEM subcutaneous NCI-H2030 xenografts NOD/SCID mice (<i>n</i> = 9/group). Azenosertib sotorasib monotherapy arms ended on days 18 27, respectively. Combination groups remained on-treatment until day 67. <i>P</i> <...
<p>Combination of azenosertib and <i>KRAS</i><sup>G12C</sup> inhibitors demonstrates synergy in NSCLC 2D <i>in vitro</i> cellular assays. <b>A,</b> Seven-day combination treatment dose matrices cell lines cultured 2D. The Loewe additivity model is depicted which scores ≥10 are synergistic. Doses expressed μmol/L. Cell arranged from most sensitive to least monotherapy (left right). <b>B,</b> Western blots protein expression...
<p>Treatment of an NSCLC model with azenosertib + sotorasib results in reduced proliferation and minor histological changes vivo.</p>
<p>Combination of azenosertib with <i>KRAS</i><sup>G12C</sup> inhibitors improves efficacy and drives tumor regression in models colorectal cancer PDAC. <b>A,</b> Percent change volume (ΔTV) individual SW837 xenografts NOD/SCID mice on day 21 treatment (<i>n</i> = 8/group). Azenosertib dosed at 60 mg/kg orally every day. Sotorasib adagrasib 30 <b>B,</b> ΔTV SW1463 NCG <b>C,</b> MIA PaCa-2 BALB/c nude 80 10 *,...