Xujun Liu

Xujun Liu


Research Focus & Metrics

Academic Career Length

2Years (2025-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 January 2025 in American Journal of Cancer Research
Verified
Journal Article
Closed access
DCDingge Cao
Dingge Cao
MWMingzhen Wang
Mingzhen Wang
YWYunyang Wang
Yunyang Wang
XHXueqing Hong
Xueqing Hong
XLXujun Liu
Xujun Liu
WSWenzhe Si
Wenzhe Si
Epigenetic modifications, particularly RNA methylation, play a crucial role in cancer progression, and N6-methyladenosine (m6A) is the most prevalent mRNA modification in eukaryotes. Wilms tumor 1-associated protein (WTAP), a key component of the m6A methyltransferase complex (MTC), regulates m6A modification, influencing RNA stability, translation, and degradation. WTAP dysregulation has been implicated in various malignancies, with particularly significant roles observed across the digestive system cancers, including but not limited to esophageal, gastric, pancreatic, gallbladder, hepatocellular, and colorectal carcinomas. Overexpression of WTAP is frequently associated with poor prognosis, advanced tumor stages, and increased metastatic potential. This review highlights the multifaceted roles and regulatory network of WTAP in digestive system cancers (DSCs) progression, encompassing tumor cell proliferation, migration, invasion, drug resistance, and immune evasion. Targeting WTAP may offer novel therapeutic strategies for overcoming therapy resistance and improving clinical outcomes in digestive system malignancies. Future research should prioritize: (1) validation of these findings in larger, multicenter, and ethnically diverse patient cohorts; (2) comprehensive elucidation of the molecular mechanisms underlying WTAP-mediated regulation in cancer biology; and (3) systematic exploration of its functional consequences in tumor progression and therapy resistance.

8 June 2026 in PeerJ
Verified
Journal Article
Open access
YCYan Chen
Yan Chen
ZWZixu Wu
Zixu Wu
WSWenzhe Si
Wenzhe Si
XLXujun Liu
Xujun Liu
In the last few years, metabolic reprogramming has been recognized as a fundamental characteristic of cancer, and is also acknowledged as a crucial cause to drug resistance, which consistently acts as a significant barrier in cancer treatment by allowing tumor cells to adapt and escape various therapies. This review gives a systematically investigation of how metabolic reprogramming contributes to drug resistance in cancer, including aerobic glycolysis (also known as the Warburg effect), lactate metabolism, glutamine addiction, lipid synthesis reprogramming, mitochondrial and ion metabolic changes. Furthermore, by clarifying the mechanisms behind these reprogrammed metabolic pathways, we explain how these changes lead to drug resistance and highlight potential molecular targets for therapeutic intervention. Additionally, we discuss emerging strategies aimed at exploiting these metabolic vulnerabilities, offering new insights for overcoming drug resistance in cancer. By integrating recent discoveries in this field, we present a unified perspective on targeting metabolic vulnerabilities to overcome drug resistance, which is an urgent need in precision oncology, and timely and concise insights for cancer biologists and researchers in the field of exploring the metabolic mechanisms of drug resistance. We hope this review will provide valuable insights for molecular tumor biologists seeking to elucidate the molecular roles of tumor metabolic reprogramming and drug resistance in cancer.

9 November 2026 in Journal of Clinical Medicine
Verified
Journal Article
Open access
PDF file
NDNan Duan
Nan Duan
JDJialin Du
Jialin Du
LWLe Wang
Le Wang
XLXujun Liu
Xujun Liu
HHHaiming Huang
Haiming Huang
BJBo Jin
Bo Jin
Objective: Respiratory tract infections (RTIs) are imposing a great economic burden, morbidity, and mortality on the healthcare system. Eleven common respiratory pathogens, based on age of onset, clinical setting, season and calendar year during and after the COVID-19 pandemic, were analyzed to optimize clinical diagnosis and prevention. Methods: In this retrospective cross-sectional study, respiratory pathogen testing results of 9882 samples from RTI patients from January 2020 to December 2025 were included to statistically analyze the positivity, distribution and trend of change. Multiplex PCR combined with capillary electrophoresis was used to simultaneously detect 11 respiratory targets. Results: The overall positive detection rate was 24.71%, with the top three pathogens being human rhinovirus (HRV) (6.20%), influenza A virus (InfA) (4.28%), and respiratory syncytial virus (RSV) (4.13%). The patients aged under 18 had the highest detection rates (≤6 years: 39.80%; 7 to 17 years: 37.95%). HRV, RSV and Mycoplasma pneumoniae (MP) were the primary pathogens among pediatric patients, while InfA was predominant in adults (including those >65 years). The 11 pathogens were most common in emergency department patients (29.14%), followed by outpatient patients (28.57%). InfA was the most predominant virus, followed by HRV and RSV, in the intensive care unit, emergency department, and outpatient settings. The detection rate was highest in autumn (33.22%), followed by winter (26.61%). MP had the highest rate in autumn, and InfA was the most frequent in winter. During the COVID-19 pandemic (2020–2022), the respiratory pathogen spectrum was dominated by HRV, RSV, and human parainfluenza virus (HPIV). And the prevalent pathogens shifted to InfA, MP and HRV during 2023–2025. Co-detections were observed in 8.03% of the positive cases, and 82.65% occurred in patients aged < 18 years. The dominant co-detections were HRV + MP, HRV + RSV and HRV + HPIV. Conclusions: The distribution of respiratory pathogens exhibited specific variations based on age, clinical setting, season, and calendar year, suggesting that differentiated prevention should be developed for different patients.