PD-L1 Cancer Research Results

PD-L1, Programmed Death-Ligand 1: Click to Expand ⟱

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PD-L1 is a protein that plays a crucial role in the regulation of the immune system. PD-L1 helps to prevent the immune system from attacking healthy cells by binding to its receptor, PD-1, on immune cells. However, some cancer cells can exploit this mechanism by expressing high levels of PD-L1, which can help them evade immune detection.
PD-L1 has become a key target for cancer immunotherapy, particularly in the development of checkpoint inhibitors.

PD-1: Upregulated on tumor-infiltrating lymphocytes (TILs), reflecting chronic antigen exposure and an “exhausted” T cell phenotype.
PD-L1 and PD-L2: Frequently overexpressed by many tumor types (e.g., non–small cell lung cancer, melanoma, renal cell carcinoma, head and neck cancers.

Scientific Papers found: Click to Expand⟱

1360-

Ash,

immuno,

Withaferin A Increases the Effectiveness of Immune Checkpoint Blocker for the Treatment of Non-Small Cell Lung Cancer

in-vitro,

Lung,

H1650

in-vitro,

Lung,

A549

in-vitro,

CRC,

HCT116

in-vitro,

BC,

MDA-MB-231

in-vivo,

NA,

mice

PD-L1↑,
eff↓, The administration of N-acetyl cysteine (NAC), a reactive oxygen species (ROS) scavenger, abrogated WFA-induced ICD and PD-L1 upregulation, suggesting the involvement of ROS in this process.
ROS↑,
ER Stress↑,
Apoptosis↑,
BAX↑,
Bak↑,
BAD↑,
Bcl-2↓,
XIAP↓,
survivin↓,
cl‑PARP↑,
CHOP↑,
p‑eIF2α↑, phosphorylation of the eukaryotic initiation factor eIF-2
ICD↑,
eff↑, WFA Sensitizes LLC Syngeneic Mouse Tumors to α-PD-L1 In Vivo

5511-

bemA,

Inhibition of ACLY overcomes cancer immunotherapy resistance via polyunsaturated fatty acids peroxidation and cGAS-STING activation

in-vitro,

Var,

ACLY↓, Here, we show that ACLY inhibition up-regulates PD-L1 immune checkpoint expression in cancer cells
PD-L1↑,
mtDam↑, Mechanistically, ACLY inhibition causes polyunsaturated fatty acid (PUFA) peroxidation and mitochondrial damage, which triggers mitochondrial DNA leakage to activate the cGAS-STING innate immune pathway.
cGAS–STING↑, ACLY inhibition leads to cGAS-STING activation
LDL↓, bempedoic acid (BemA; also named ETC-1002) has been recently approved by U.S. Food and Drug Administration (FDA) for lowering low-density lipoprotein cholesterol
eff↑, dietary PUFA supplementation is sufficient to mimic the enhanced efficacy of PD-L1 blockade by ACLY inhibition, providing promising combinational strategies for immunotherapy-resistant tumors therapy.

741-

Bor,

Boron Derivatives Inhibit the Proliferation of Breast Cancer Cells and Affect Tumor-Specific T Cell Activity In Vitro by Distinct Mechanisms

in-vitro,

BC,

MCF-7

in-vitro,

BC,

MDA-MB-231

MOB1↓,
PD-L1↑,
p‑YAP/TEAD↝,
IFN-γ↓,
sFasL↑,
Perforin↓,
GranA↓,
GranB↓,
GNLY↓,
PD-1↑, increased the expression of PD-1 surface protein in activated T cells

5845-

CAP,

Unveiling the Molecular Mechanisms Driving the Capsaicin-Induced Immunomodulatory Effects on PD-L1 Expression in Bladder and Renal Cancer Cell Lines

in-vivo,

RCC,

A498

in-vitro,

RCC,

T24/HTB-9

NA,

Bladder,

5637

TRPV1↑, CPS has been found to induce both carcinogenic and anti-carcinogenic effects in a transient receptor potential vanilloid subtype 1 (TRPV1)-dependent and -independent manner [7,8,9,10,11].
TumCP↓, CPS at high doses reduces proliferation of RCCs in a TRPV1-dependent manner, induces caspase-dependent apoptosis and growth of 786-O RC xenografts in vivo
Casp↑,
Apoptosis↑,
SIRT1↓, Moreover, by downregulating SIRT1, CPS enhances the acetylation of cortactin and β-catenin to decrease MMP-2 and MMP-9 activation and impair cell migration in BC cells [15,16].
MMP2↓,
MMP9↓,
TumCMig↓,
TumCCA↑, CPS suppresses cell proliferation, and induces cell cycle arrest and reactive oxygen species (ROS) production in BC cells, through FOXO3a-mediated pathways [17,18].
ROS↑,
DNAdam↑, CPS Induces DNA Damage in Living 5637, T24 and A498 Cancer Cell Lines
PD-L1↑, We found that CPS increased the PD-L1 expression, both at mRNA and protein levels, in T24 and 5637 cells
eff↓, ROS generation was completely reverted by NAC in CPS-treated A498 cells at 3–6 h treatment

4916-

DSF,

Cu,

The immunomodulatory function and antitumor effect of disulfiram: paving the way for novel cancer therapeutics

Review,

Var,

TumCP↓, inhibits proliferation, migration, and invasion of malignant tumor cells.
TumCMig↓,
TumCI↓,
eff↑, divalent copper ions can enhance the antitumor effects of DSF
Imm↑, immunomodulatory properties of DSF
ROS↑, Elevated production of reactive oxygen species (ROS) and suppression of the ROS/NF-κB signaling pathway
NF-kB↓,
chemoP↑, DSF has been shown to effectively inhibit NF-κB pathway activity and augment the apoptotic impact of 5-fluorouracil (5-FU) on colorectal cancer cells when administered in conjunction with 5-FU
JNK↑, Activate the JNK signaling pathway
FOXO↑, In acute myeloid leukemia, DSF/Cu2+ enhances the expression of the oncogene FOXO and inhibits the expression of the oncogene MYC, inducing G0/G1 cell cycle arrest and tumor cell apoptosis
Myc↑,
TumCCA↑,
Apoptosis↑,
RadioS↑, DSF/Cu2+ enhances the efficacy of conventional chemotherapy and chemoradiation, while remaining cost-effective
PD-L1↑, DSF can upregulate PD-L1 expression by promoting DNMT1-mediated hypomethylation of IRF7
eff↑, DSF was found to markedly enhance the efficacy of anti-PD-1 antibody treatment
CSCs↓, Inhibition of cancer stem cells
Dose↝, DSF's oral dosage form is ineffective for cancer treatment due to its instability in the gastric environment and rapid degradation in the body
Half-Life↑, DSF encapsulated PEG-PLGA NPs have been shown to improve tumor site delivery and prolong systemic circulation half-life.

1040-

LE,

Licorice extract inhibits growth of non-small cell lung cancer by down-regulating CDK4-Cyclin D1 complex and increasing CD8+ T cell infiltration

in-vivo,

Lung,

H1975

5400 μg/mL

mice

TumCCA↑, G0/G1 growth phase cycle arrest
CDK4↓,
cycD1/CCND1↓,
PD-L1↑, increased PD-L1 levels in lung cancer cells
TumVol↓,

516-

MFrot,

immuno,

MF,

Anti-tumor effect of innovative tumor treatment device OM-100 through enhancing anti-PD-1 immunotherapy in glioblastoma growth

vitro+vivo,

GBM,

U87MG

1mT, 120Hz (7200rpm), 24, 48, and 72 h

OM‑100 device (motor driven pulses)

TumCP↓,
Apoptosis↑,
TumCMig↓,
ROS↑, treatment with OM-100 led to an increase in intracellular ROS levels
PD-L1↑, upregulating PD-L1 expression, thereby enhancing the efficacy of anti-PD-1 immunotherapy
TumVol↓, in mice
eff↑, enhance the efficacy of anti‑PD‑1 immunotherapy in vivo
*toxicity∅, OM-100 did not result in noteworthy changes in the blood routine parameters (Gran, HCT, HGB, Lymph, MCH, MCV, PLT, RBC, MPV, and WBC) and biochemical indicators (ALT, AST, T-BIL, CREA, TG, TC, HDL-c, and LDL-c) in normal mice
eff↑, Particularly, there was a more pronounced response to anti-PD-1 therapy in patients whose tumors expressed PD-L1 3
*toxicity∅, OM-100 treatment in healthy mice showed no adverse effects, indicating its safety for normal tissues.
Dose↝, 24-day treatment with a magnetic field intensity of 1.066 mT and a frequency of 100 kHz (figure shows motor driven 120Hz, 7200rpm pulsed
tumCV↓, anti-tumor efficacy of OM-100 treatment, which by impairing cell viability, increasing apoptosis, inhibiting cell migration, and invasion capabilities, as well as promoting oxidative stress.
TumCI↓,

1047-

RES,

Resveratrol induces PD-L1 expression through snail-driven activation of Wnt pathway in lung cancer cells

in-vitro,

Lung,

H1299

below 5 μM

in-vitro,

Lung,

A549

in-vitro,

Lung,

H460

PD-L1↑, resveratrol dose-dependently upregulates PD-L1 expression at the range of pharmacologic-achievable concentrations in lung cancer cells
Snail↑, resveratrol dose-dependently increased Snail levels in association with the suppression of E-cadherin protein levels, as well as induction of N-cadherin, Fibronectin and Vimentin levels
E-cadherin↓,
N-cadherin↑, induction of N-cadherin, Fibronectin and Vimentin levels
Fibronectin↑,
Vim↑,
Axin2↓, Snail in turn inhibits transcription of Axin2

Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes ⓘ

chemoP↑, 1, TumVol↓, 2,
Total Targets: 61

Pathway results for Effect on Normal Cells:

Functional Outcomes ⓘ

toxicity∅, 2,
Total Targets: 1

Scientific Paper Hit Count for: PD-L1, Programmed Death-Ligand 1

2 immunotherapy
1 Ashwagandha(Withaferin A)
1 bempedoic acid
1 Boron
1 Capsaicin
1 Disulfiram
1 Copper and Cu NanoParticles
1 Licorice
1 Magnetic Field Rotating
1 Magnetic Fields
1 Resveratrol

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:243  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

PD-L1 Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Immune & Inflammatory Signaling ⓘ

Cellular Microenvironment ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Functional Outcomes ⓘ

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