M2 MC Cancer Research Results

M2 MC, M2 macrophage conversion: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
M2 macrophages (M2 MC) are a subtype of macrophages that are generally associated with anti-inflammatory responses, tissue repair, and the promotion of tumor growth.
Strategies to reprogram M2 macrophages into a more pro-inflammatory M1 phenotype or to inhibit their function are being explored in cancer therapies.
M2 macrophages can play a dual role, promotion/suspression.
M2 macrophages are a subtype of macrophages that are generally associated with anti-inflammatory responses, tissue repair, and the promotion of tumor growth. The conversion of macrophages from the M1 (pro-inflammatory) to the M2 (anti-inflammatory) phenotype is a critical process in the tumor microenvironment and has significant implications for cancer progression.

M2 macrophages are generally considered protumorigenic. They secrete various cytokines and growth factors that promote tumor cell proliferation, angiogenesis, and tissue remodeling. Additionally, they can suppress the activity of cytotoxic T cells and natural killer (NK) cells, further aiding tumor immune evasion.
PC, Pancreatic Cancer: Click to Expand ⟱
Pancreatic Cancer: Hypoxia (low oxygen tension) is commonly found in solid tumors. Hypoxia-inducible factor-1 (HIF-1),is a key mediator of the cellular response to hypoxia and is overexpressed in a wide variety of solid tumors, including pancreatic cancer.
Nanog is highly expressed in CSCs compared to normal cells [93–97]
HIF-1↑
Scientific Papers found: Click to Expand⟱
1577- Citrate,    Citric acid promotes SPARC release in pancreatic cancer cells and inhibits the progression of pancreatic tumors in mice on a high-fat diet
- in-vivo, PC, NA - in-vitro, PC, PANC1 - in-vitro, PC, PATU-8988 - in-vitro, PC, MIA PaCa-2
Apoptosis↑, TumCP↓, TumCG↑, SPARC↑, Glycolysis↓, OCR↓, pol-M1↑, pol-M2 MC↓, Weight∅, ATP↓, ECAR↓, mitResp↓, i-ATP↑, p65↓, i-Ca+2↑, eff↓,
7776- IBC,    Isobavachalcone Activates Antitumor Immunity on Orthotopic Pancreatic Cancer Model: A Screening and Validation
- vitro+vivo, PC, Panc02
TumCP↓, Apoptosis↑, ROS↑, TumW↓, CD8+↑, M2 MC↓, CSCs↓, antiNeop↑, Imm↑, eff↓, Bcl-2↓, BAX↑,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 1,   i-ATP↑, 1,   mitResp↓, 1,   OCR↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ECAR↓, 1,   Glycolysis↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 2,   BAX↑, 1,   Bcl-2↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

CSCs↓, 1,   TumCG↑, 1,  

Migration(tgid=13) ⓘ

i-Ca+2↑, 1,   SPARC↑, 1,   TumCP↓, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Imm↑, 1,   pol-M1↑, 1,   M2 MC↓, 1,   pol-M2 MC↓, 1,   p65↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↓, 2,  

Functional Outcomes(tgid=23) ⓘ

antiNeop↑, 1,   TumW↓, 1,   Weight∅, 1,  

Infection & Microbiome(tgid=24) ⓘ

CD8+↑, 1,  
Total Targets: 25

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: M2 MC, M2 macrophage conversion
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:21  Cells:%  prod#:%  Target#:177  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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