Mingming Zheng

ORCID: 0000-0002-8415-0078
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Research Areas
  • Adenosine and Purinergic Signaling
  • Cancer, Lipids, and Metabolism
  • Cancer Immunotherapy and Biomarkers
  • RNA Interference and Gene Delivery
  • Immune Cell Function and Interaction
  • Transplantation: Methods and Outcomes
  • Plant biochemistry and biosynthesis
  • Ubiquitin and proteasome pathways
  • Cancer-related gene regulation
  • Cancer, Hypoxia, and Metabolism
  • Endoplasmic Reticulum Stress and Disease
  • Kruppel-like factors research
  • Natural Products and Biological Research
  • Epigenetics and DNA Methylation
  • Mangiferin and Mango Extracts
  • Inflammasome and immune disorders
  • Autophagy in Disease and Therapy
  • Phagocytosis and Immune Regulation

Zhejiang University
2022-2024

Royal Society of Chemistry
2024

Centre National pour la Recherche Scientifique et Technique (CNRST)
2024

Zhejiang Pharmaceutical College
2023

Abstract The intracellular distribution and transportation process are essential for maintaining PD‐L1 (programmed death‐ligand 1) expression, intervening in this cellular may provide promising therapeutic strategies. Here, through a cell‐based high content screening, it is found that the ABCB1 (ATP binding cassette subfamily B member modulator zosuquidar dramatically suppresses expression by triggering its autophagic degradation. Mechanistically, interacts with impairs COP II‐mediated...

10.1002/advs.202400340 article EN cc-by Advanced Science 2024-09-04

Mevalonate metabolism plays an important role in regulating tumor growth and progression; however, its immune evasion checkpoint modulation remains unclear. Here, we found that non-small cell lung cancer (NSCLC) patients with higher plasma mevalonate response better to anti-PD-(L)1 therapy, as indicated by prolonged progression-free survival overall survival. Plasma levels were positively correlated programmed death ligand-1 (PD-L1) expression tissues. In NSCLC lines patient-derived cells,...

10.1016/j.apsb.2023.04.002 article EN cc-by-nc-nd Acta Pharmaceutica Sinica B 2023-04-17

Adenosine (Ado) is significantly elevated in the tumor microenvironment (TME) compared to normal tissues. It binds adenosine receptors (AdoRs), suppressing antigen presentation and immune cell activation, thereby inhibiting adaptive immunity. Ado downregulates major histocompatibility complex II (MHC II) co-stimulatory factors on Dendritic cells (DCs) macrophages, presentation. suppresses anti-tumor cytokine secretion T activation by disrupting receptor (TCR) binding signal transduction....

10.1016/j.apsb.2023.12.004 article EN cc-by-nc-nd Acta Pharmaceutica Sinica B 2023-12-16

Recent studies have pointed to the role of Krüpple‐like factor 12 (KLF12) in cancer‐associated processes, including cancer proliferation, apoptosis, and metastasis. However, KLF12 tumor immunity remains obscure. Here, we found that expression was significantly higher non‐small cell lung (NSCLC) cells with programmed death‐ligand 1 ( PD‐L1 ) expression. Additionally, a positive correlation between observed clinical patient tissues. By chromatin immunoprecipitation (ChIP) analysis, identified...

10.1002/1878-0261.13512 article EN cc-by Molecular Oncology 2023-08-22

Adenosine (Ado), mainly produced by the hydrolysis of ATP, exhibits significantly elevated levels in tumor microenvironment (TME) compared to normal tissues. Upon binding adenosine receptors (AdoRs), Ado initiates downstream signaling pathways that suppress antigen presentation and immune cell activation, thereby inhibiting adaptive immunity. downregulates major histocompatibility complex II (MHC II) co-stimulatory factors expression on DCs macrophages, T cells. inhibits receptor (TCR) its...

10.22541/au.168838779.94228226/v1 preprint EN Authorea (Authorea) 2023-07-03
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