Zhicheng Wang

Prof. Zhicheng Wang


Research Focus & Metrics

Academic Career Length

4Years (2023-Present)

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

Representative Publications

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25 June 2023 in Advanced Science
Verified
Journal Article
Open access
YGYixiao Gan
Yixiao Gan
GZGang Zhao
Gang Zhao
ZWZhicheng Wang
Zhicheng Wang
XZXingcai Zhang
Xingcai Zhang
Mei X. WuMei X. Wu
Mei X. Wu
MLMin Lu
Min Lu
Bacterial or fungal membrane vesicles, traditionally considered as microbial metabolic wastes, are secreted mainly from the outer membrane or cell membrane of microorganisms. However, recent studies have shown that these vesicles play essential roles in direct or indirect communications among microorganisms and between microorganisms and hosts. This review aims to provide an updated understanding of the physiological functions and emerging applications of bacterial membrane vesicles, with a focus on their biogenesis, mechanisms of adsorption and invasion into host cells, immune stimulatory effects, and roles in the much‐concerned problem of bacterial resistance. Additionally, the potential applications of these vesicles as biomarkers, vaccine candidates, and drug delivery platforms are discussed.

Verified
Journal Article
Open access
PDF file
YWYan Wang
Yan Wang
BCBowei Cao
Bowei Cao
HLHuili Lu
Huili Lu
ZWZhicheng Wang
Zhicheng Wang
YQYanli Qin
Yanli Qin
Tumor cells possess nucleic-acid sensing systems that detect aberrant DNA and RNA arising from genomic and transcriptomic dysregulation. Cytosolic DNA and RNA sensors, together with endosomal nucleic acid sensors, can induce type I interferons, inflammatory chemokines, antigen presentation programs, and immune cell recruitment. Yet many tumors remain immunologically silent despite harboring potentially immunostimulatory nucleic acids, indicating that malignant cells can restrain these pathways at multiple levels. Nucleic acid clearance, selective RNA editing and remodeling, extracellular second messenger degradation, and epigenetic silencing can suppress these responses. These regulatory layers may favor immune-poor tumor states and limit responsiveness to immune checkpoint blockade. Therapeutic reactivation must be spatially and temporally controlled, because persistent signaling can undergo maladaptive rewiring. We review these molecular brakes, therapeutic strategies to restore innate sensing, and a proposed biomarker framework integrating sensor competence, suppressor activity, and functional immune output. We distinguish the effects arising within tumor cells from those mediated by sensing mechanisms in neighboring host cells and discuss cellular and spatial context, signaling dynamics, and safety. The proposed framework for matching treatments to patients remains investigational and requires prospective clinical validation.