Shensi Shen

ORCID: 0000-0002-5087-8220
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About
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Research Areas
  • Cancer Immunotherapy and Biomarkers
  • Autophagy in Disease and Therapy
  • Immunotherapy and Immune Responses
  • CAR-T cell therapy research
  • RNA and protein synthesis mechanisms
  • Adenosine and Purinergic Signaling
  • RNA modifications and cancer
  • CRISPR and Genetic Engineering
  • Biological Activity of Diterpenoids and Biflavonoids
  • Cancer, Hypoxia, and Metabolism
  • RNA Research and Splicing
  • Cancer Research and Treatments
  • Endoplasmic Reticulum Stress and Disease
  • Melanoma and MAPK Pathways
  • Immune Cell Function and Interaction
  • Advanced biosensing and bioanalysis techniques
  • Cytokine Signaling Pathways and Interactions
  • Synthesis of Organic Compounds
  • RNA Interference and Gene Delivery
  • Phenothiazines and Benzothiazines Synthesis and Activities
  • Cancer Genomics and Diagnostics
  • Cancer-related Molecular Pathways
  • Ferroptosis and cancer prognosis
  • Calcium signaling and nucleotide metabolism
  • Epigenetics and DNA Methylation

West China Hospital of Sichuan University
2021-2025

Sichuan University
2021-2025

Institut Gustave Roussy
2009-2023

Inserm
2009-2023

Chinese Academy of Sciences
2009-2023

Shanghai Institute of Materia Medica
2011-2023

Robert Bosch (Germany)
2023

Chengdu University
2022

West China Medical Center of Sichuan University
2021

Université d'Évry Val-d'Essonne
2013-2020

Antineoplastic chemotherapies are particularly efficient when they elicit immunogenic cell death, thus provoking an anticancer immune response. Here we demonstrate that autophagy, which is often disabled in cancer, dispensable for chemotherapy-induced death but required its immunogenicity. In response to chemotherapy, autophagy-competent, not autophagy-deficient, cancers attracted dendritic cells and T lymphocytes into the tumor bed. Suppression of autophagy inhibited release adenosine...

10.1126/science.1208347 article EN Science 2011-12-15

Autophagy protects organelles, cells, and organisms against several stress conditions. Induction of autophagy by resveratrol requires the nicotinamide adenine dinucleotide–dependent deacetylase sirtuin 1 (SIRT1). In this paper, we show that acetylase inhibitor spermidine stimulates independent SIRT1 in human yeast cells as well nematodes. Although ignite through distinct mechanisms, these compounds stimulate convergent pathways culminate concordant modifications acetylproteome. Both agents...

10.1083/jcb.201008167 article EN cc-by-nc-sa The Journal of Cell Biology 2011-02-21

Keeping Cancer Cells At Bay cells are often aneuploid; that is, they have an abnormal number of chromosomes. But to what extent this contributes the tumorigenic phenotype is not clear. Senovilla et al. (p. 1678 ; see Perspective by Zanetti and Mahadevan ) found tetraploidization cancer can cause them become immunogenic thus aid in their clearance from body immune system. with excess chromosomes put stress on endoplasmic reticulum, which leads movement protein calreticulin cell surface....

10.1126/science.1224922 article EN Science 2012-09-28

Macroautophagy is known to participate in the quality control and turnover of cytoplasmic organelles, yet there little evidence that macroautophagy targets nuclei mammalian cells. Here, we investigated whether autophagy may target micronuclei, which arise as a result deficient bipolar chromosome segregation cells exposed cell cycle perturbations. After removal several distinct blockers (nocodazole, cytochalasin D, hydroxyurea or SP600125), manifested an increase frequency micronuclei...

10.4161/cc.11.1.18564 article EN Cell Cycle 2012-01-01

The tumor suppressor protein p53 tonically suppresses autophagy when it is present in the cytoplasm. This effect phylogenetically conserved from mammals to nematodes, and human can inhibit yeast, as we show here. Bioinformatic investigations of interactome relationship autophagy-relevant network underscored possible relevance a direct molecular interaction between mammalian ortholog essential yeast Atg17, namely RB1-inducible coiled-coil 1 (RB1CC1), also called FAK family kinase-interacting...

10.4161/cc.10.16.16868 article EN Cell Cycle 2011-08-15

SummaryPatients with non-small cell lung cancer (NSCLC) are routinely treated cytotoxic agents such as cisplatin. Through a genome-wide siRNA-based screen, we identified vitamin B6 metabolism central regulator of cisplatin responses in vitro and vivo. By aggravating bioenergetic catastrophe that involves the depletion intracellular glutathione, exacerbates cisplatin-mediated DNA damage, thus sensitizing large panel lines to apoptosis. Moreover, sensitizes cells apoptosis induction by...

10.1016/j.celrep.2012.06.017 article EN cc-by-nc-nd Cell Reports 2012-07-26

Emerging evidence indicates that non-mutational drug tolerance mechanisms underlie the survival of residual cancer "persister" cells. Here, we find BRAF(V600E) mutant melanoma persister cells tolerant to BRAF/MEK inhibitors switch their metabolism from glycolysis oxidative respiration supported by peroxisomal fatty acid β-oxidation (FAO) is transcriptionally regulated peroxisome proliferator-activated receptor alpha (PPARα). Knockdown key FAO enzyme, acyl-CoA oxidase 1 (ACOX1), as well...

10.1016/j.celrep.2020.108421 article EN cc-by-nc-nd Cell Reports 2020-11-01

One particular strategy to render anticancer therapies efficient consists of converting the patient’s own tumor cells into therapeutic vaccines, via induction immunogenic cell death (ICD). hallmarks ICD dwells in active release ATP by committed undergo, but not yet having succumbed to, apoptosis. We observed that knockdown essential autophagy-related genes (ATG3, ATG5, ATG7 and BECN1) abolishes pre-apoptotic secretion several human murine cancer lines undergoing ICD. Accordingly,...

10.4161/auto.19009 article EN Autophagy 2012-03-19

Constitutive activation of the Janus kinase (JAK)/signal transducer and activator transcription (STAT) pathway occurs frequently in cancer cells contributes to oncogenesis. Among members STAT family, STAT3 plays a pivotal role development progression human tumors. The STAT3-mediated signaling has been recognized as promising anticancer target. Here, we show that 17-Hydroxy-jolkinolide B (HJB), diterpenoid from Chinese medicinal herb Euphorbia fischeriana Steud, strongly inhibits interleukin...

10.1158/0008-5472.can-09-0462 article EN Cancer Research 2009-08-26

Abstract Cancer persister cells tolerate anticancer drugs and serve as the founders of acquired resistance cancer relapse. Here we show that a subpopulation BRAF V600 mutant melanoma tolerates exposure to MEK inhibitors undergoes reversible remodelling mRNA translation evolves in parallel with drug sensitivity. Although this process is associated global reduction protein synthesis, subset mRNAs an increased efficiency translation. Inhibiting eIF4A RNA helicase, component eIF4F initiation...

10.1038/s41467-019-13360-6 article EN cc-by Nature Communications 2019-12-16

<ns4:p>In this review, we propose a recension of biological observations on plasticity in cancer cell populations and discuss theoretical considerations about their mechanisms.</ns4:p>

10.12688/f1000research.24803.1 preprint EN cc-by F1000Research 2020-06-22
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