About

Xiaojing Ma is a researcher whose work focuses on the molecular mechanisms underlying cancer progression, metastasis, and immune evasion. Her research includes studying the role of ubiquitin ligases such as UBR5 in promoting tumor growth and metastasis, as well as investigating how tumor cells evade immune responses through various signaling pathways. Her contributions extend to understanding the regulation of cytokine production, macrophage polarization, and the tumor microenvironment, with a particular emphasis on the molecular interactions that facilitate cancer cell survival and dissemination. Ma's work also explores targeted therapies and nanotherapies for pancreatic neuroendocrine tumors and breast cancer, highlighting her commitment to developing novel strategies for cancer treatment.

Research topics

• Immunology
• Biology
• Cancer research
• Biochemistry
• Cell biology

Selected publications

• ANKRD53 is downregulated in human obesity and coordinates lipolysis with mitochondrial oxidative metabolism in adipocytes

  Molecular Metabolism · 2026-02-05

  articleOpen accessCorresponding

  Human adipose tissue is central to obesity‐associated metabolic dysfunction. ANKRD53 is a human‐specific, adipocyte‐enriched ankyrin repeat scaffold protein with largely unknown function. We investigated its role in human adipocyte metabolism and the underlying mechanism. RNA-seq analysis of subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) from 236 individuals quantified ANKRD53 expression and its association with metabolic traits. In human primary adipocytes, we assessed lipolysis (free fatty acid and glycerol release) and mitochondrial respiration (oxygen consumption rate) after ANKRD53 overexpression or knockdown. An AAV was used to overexpress ANKRD53 in mouse inguinal white adipose tissue (iWAT). Protein interactors were identified by immunoprecipitation–mass spectrometry, and knockdown experiments confirmed a functional role of ACSL1. ANKRD53 expression in both adipose depots was markedly reduced in obesity and inversely correlated with BMI, adiposity measures, insulin resistance indices, and circulating triglycerides, while positively associated with adiponectin and HDL. In human adipocytes, ANKRD53 overexpression enhanced forskolin-stimulated lipolysis and mitochondrial respiration, whereas silencing impaired these processes. Adipose-targeted ANKRD53 overexpression in mice increased lipolysis in vivo. Mechanistically, ANKRD53 interacted with ACSL1 and promoted its mitochondrial localization, channeling lipolysis-derived FFAs into β-oxidation; silencing ACSL1 abrogated ANKRD53’s effects. ANKRD53 is reduced in obesity and coordinates lipolysis with mitochondrial oxidative metabolism in human adipocytes, promoting efficient use of lipolysis-derived FFAs via ACSL1. These findings establish ANKRD53 as a key regulator of adipocyte energy metabolism and a potential therapeutic target for improving metabolic health in obesity. • ANKRD53 expression is reduced in obesity and inversely correlated with adiposity and metabolic risk measures. • ANKRD53 is uniquely expressed in human adipocytes but undetectable in mouse adipose tissue. • In human primary adipocytes, ANKRD53 enhances lipolysis and mitochondrial respiration. • ANKRD53 interacts with ACSL1 to channel lipolysis-derived fatty acids into mitochondria, linking lipid mobilization to mitochondrial oxidative metabolism.

  PublisherDOI

• Preconception One‐Carbon Metabolism Nutrient Levels in Preparing for Pregnancy Couples and Spontaneous Pregnancy Loss: A Prospective Cohort Study

  MedComm · 2026-03-30

  articleOpen access

  Spontaneous pregnancy loss (SPL) remains an important yet poorly understood pregnancy outcome. One-carbon metabolism (OCM) nutrients play an essential role in embryonic development, but their relationship with SPL remains unclear. In this prospective cohort of 11,033 couples and 2862 unpaired mothers, we assessed associations between preconception parental one-carbon metabolism (OCM) nutrients and SPL risk. We used generalized linear models to estimate risk ratios (RRs) and 95% confidence intervals (CIs) for fathers, mothers, and the combined parental population, respectively. Each 100 ng/mL increase in paternal and maternal red blood cell (RBC) folate was associated with a 19% (aRR = 0.81; 95% CI, 0.73-0.90) and an 8% (aRR = 0.92; 0.85-0.98) lower SPL risk, respectively. The risk was reduced by 64% (aRR = 0.36; 0.16-0.79) when both parents achieved levels ≥ 400 ng/mL, compared to neither. Exploratory case-control analysis suggested associations of parental serum betaine with increased risk of SPL (β [standard error]: 0.09 [0.11] for fathers; 0.02 [0.08] for mothers) and inverse associations for taurine (-0.09 [0.11] and -0.03 [0.08], respectively). These findings highlight paternal and maternal preconception RBC folate, and imbalances in OCM metabolites are associated with an increased SPL risk, offering novel insights into SPL etiology and have public health implications.

  PublisherDOI

• Nanowire-Mediated Eradication of Polymicrobial Biofilms

  ACS Omega · 2026-02-05

  articleOpen access1st author

  Streptococcus pneumoniae (S. pneumoniae) and Nontypeable Hemophiles influenzae (NTHi) are two of the most common pathogens causing otitis media (OM), which is the primary reason for pediatric antibiotic prescriptions. They have been shown to coexist and, in some cases, form biofilms that are resistant to antibiotics, causing recurrent or chronic OM. The current treatment regimen requires a rigorous course of multidose antibiotics over 5–10 days, which is nevertheless found insufficient to eradicate the polymicrobial biofilms. To tackle this challenge, we utilized a nanozyme, i.e., vanadium pentoxide nanowires (V2O5 NWs), to convert a metabolic product (H2O2) of S. pneumoniae into a potent antiseptic (HOBr), thus eradicating polymicrobial biofilms comprising S. pneumoniae and NTHi. Interestingly, when V2O5 NWs were combined with conventional antibiotics (i.e., ciprofloxacin and moxifloxacin), they exhibited synergistic effects against monocultured pathogens, as demonstrated using isobologram analysis. Against S. pneumoniae, regardless of mono- or coculture, additive effects were observed, with the exception of the levofloxacin-ciprofloxacin pair, which resulted in antagonistic effects in cocultured conditions. The strategies developed in this study, therefore, have the potential to tackle polymicrobial OM, biofilm-induced infections and associated antimicrobial resistance while reducing the overall antibiotic exposure incurred by OM.

  PublisherDOI

• Essential role of NONO-HOXA1-Wnt axis in cardiomyocyte differentiation

  Nature Communications · 2026-01-24

  articleOpen access

  NONO is recognized as a critical molecular scaffold involved in both transcriptional and posttranscriptional regulation. Mutations in NONO are frequently linked to congenital heart diseases (CHDs) in humans. However, the mechanisms by which NONO regulates cardiac development remain elusive. Here, we identified NONO as a pivotal dual-function regulator of cardiomyocyte differentiation in human induced pluripotent stem cells (hiPSCs). NONO deficiency in hiPSCs results in a distinct defect in early cardiomyocyte differentiation. Mechanistically, NONO interacts with HOXA1 and regulates the dynamic expression of key genes during early cardiomyocyte differentiation. ChIP-seq analysis reveals that NONO loss reduces HOXA1 occupancy at target genes, compromising its transcriptional regulation. Additionally, NONO and HOXA1 cooperatively activate the Wnt signaling. Taken together, these findings establish the NONO-HOXA1-Wnt axis as a key molecular mechanism in cardiomyocyte differentiation and provide insights into the etiology of CHDs associated with NONO mutations.

  PublisherDOI

• Glycemic Variability Bridges Time in Range and Time in Tight Range: A Unified Equation for Both Type 1 and Type 2 Diabetes Based on Large‐Scale Continuous Glucose Monitoring Data

  Diabetes Obesity and Metabolism · 2026-03-27 · 1 citations

  articleOpen access

  ABSTRACT Aims This study aimed to establish a regression model for the relationship between time in range (TIR) and time in tight range (TITR) in individuals with type 1 diabetes (T1D) and type 2 diabetes (T2D) based on real‐world continuous glucose monitoring (CGM) data. Materials and Methods A cross‐sectional analysis was conducted on over 200 000 CGM users with diabetes. Participants self‐reported basic demographic and clinical details via in‐app fields. Exponential regression models were constructed to examine the TIR‐TITR association for individuals with T1D and T2D, respectively. After controlling for coefficient of variation (CV), the model was extended to provide more precise glycemic targets for clinical use. Model performance was evaluated using the coefficient of determination ( R 2 ), root mean square error (RMSE), and Akaike information criterion (AIC). Results The TIR‐TITR relationship exhibited a nonlinear relationship. Exponential models (TITR T1D = 8.54436 × exp[0.02414 × TIR]; TITR T2D = 5.52189 × exp[0.02839 × TIR]) provided the best fit compared to linear and quadratic models. A TIR of 70% corresponded to TITR values of 40.3%–46.3%, whereas achieving TITR of 50% required TIR of 73.2%–77.6%. For TIR below 60%, each 5% TIR increment boosted TITR by less than 5% points; above 60%, gains exceeded 5% points. Additionally, the inclusion of CV in the model was associated with reduced differences between the fitted T1D and T2D curves and improved the model's performance (TITR = 2.18448 × exp[0.03749 × TIR] +0.94018 × CV−14.99420). Conclusions This study established the exponential model for TIR‐TITR relationship in individuals with T1D and T2D, using a real‐world CGM dataset. The model may provide new insights into the setting of individualized treatment goals.

  PublisherDOI

• Pheochromocytoma-Induced Angina Pectoris Mimicking Acute Coronary Syndrome

  The American Journal of Medicine · 2026-04-01

  articleSenior author
  PublisherDOI

• Comparable performance of 1,5-anhydroglucitol and continuous glucose monitoring in detecting subclinical atherosclerosis in elderly patients with type 2 diabetes

  Cardiovascular Diabetology · 2025-11-21 · 1 citations

  articleOpen access

  The comparison between conventional glycemic markers and continuous glucose monitoring (CGM) in relation to adverse outcomes in the elderly with type 2 diabetes remains unclear. We aimed to assess associations of 1,5-anhydroglucitol (1,5-AG) and CGM metrics with carotid intima-media thickness (CIMT) as a surrogate of cardiovascular disease. The study included 2509 adults aged ≥ 60 years with type 2 diabetes. CIMT was measured by high-resolution ultrasonography, with abnormal CIMT defined as a mean thickness of ≥ 1.0 mm. Time in range (TIR), mean sensor glucose (MSG), time above range (TAR, > 10.0 mmol/L), standard deviation (SD), and coefficient of variation (CV) were calculated from CGM data. The median serum 1,5-AG was 3.9 (2.0, 8.0) μg/mL, and the prevalence of abnormal CIMT was 44.2% (n = 1,109). The prevalence of abnormal CIMT decreased across ascending 1,5-AG categories (P for trend < 0.01). In the fully adjusted model, each 1-standard deviation decrease in 1,5-AG conferred 10% higher odds of abnormal CIMT. Compared with 1,5-AG ≥ 10.0 μg/mL, 1,5-AG < 6.0 μg/mL was associated with an odds ratio of 1.25 (95% CI 1.00–1.55) for abnormal CIMT. Among CGM metrics, TIR, MSG, and TAR > 10.0, but not CV or SD, were significantly associated with abnormal CIMT. The C-statistics for 1,5-AG in predicting abnormal CIMT were comparable to those for TIR, MSG, and TAR >10.0 (all P > 0.05). In older adults with type 2 diabetes, 1,5-AG demonstrated a performance comparable to CGM for detecting abnormal CIMT, supporting its potential as a clinical biomarker for identifying subclinical atherosclerosis.

  PublisherOA PDFDOI

• Recent advances on electrocatalytic hydrodechlorination of chlorinated organic pollutants

  Surfaces and Interfaces · 2025-10-01

  article1st author
  PublisherDOI

• Acetaldehyde dehydrogenase 1A1 upregulation drives dacomitinib-induced skin toxicity through mitochondrial dysfunction and keratinocyte apoptosis

  Cellular Signalling · 2025-06-03 · 2 citations

  article
  PublisherDOI

• Self-nanoemulsifying delivery system of PEITC ameliorates DSS-induced ulcerative colitis by regulating NF-κB pathway, modulating oxidative stress, and barrier repair

  Food Bioscience · 2025-09-24 · 1 citations

  articleSenior authorCorresponding
  PublisherDOI

Recent grants

• NIH Grant R21AT004349

  NIH · $431k · 2010

• NIH Grant R56AI103157

  NIH · $424k · 2016

• NIH Grant R01CA100223

  NIH · $1.5M · 2010

• NIH Grant R01AI072149

  NIH · $857k · 2012

• NIH Grant R01AI045899

  NIH · $3.0M · 2010

Frequent coauthors

• Giorgio Trinchieri

  Fox Chase Cancer Center

  97 shared

• Salem Chouaı̈b

  Gulf Medical University

  73 shared

• Sandra Pellegrini

  72 shared

• F. Gay

  University of Naples Federico II

  72 shared

• Patrick Mayeux

  72 shared

• Cécile Pardoux

  72 shared

• Stéphanie Gobert

  Université Claude Bernard Lyon 1

  72 shared

• Mei Song

  Zhejiang Cancer Hospital

  70 shared

Education

• PhD, Genetics

  University of Edinburgh

  1987

• B.S., Animal Science

  China Agricultural University

  1982