Hi, Continue visiting your profile
user

Login

Email

Password

Create account
Forget password
do you want to Log Out ?
AnyGenes

TUMOR MICROENVIRONMENT

The tumor microenvironment (TME) is a complex and dynamic ecosystem surrounding tumor cells, composed of various components like extracellular matrix (ECM), blood vessels, immune cells, fibroblasts, and signaling molecules. The TME plays a crucial role in tumor growth, metastasis, and resistance to treatment, making it an essential area of research in cancer biology.

AnyGenes offers advanced qPCR array products that enable comprehensive analysis of genes involved in the tumor microenvironment. These arrays are designed to help researchers investigate the critical biomarkers and signaling pathways that contribute to cancer progression, metastasis, and immune response. By using AnyGenes' qPCR arrays, you can gain valuable insights into the molecular mechanisms of the TME and enhance your research on cancer therapies.

Investigating tumor microenvironment components using AnyGenes qPCR array for cancer research.
Hormones, metabolites and cytokines released by the microenvironment regulate gene expression to increase glucose uptake and glycolysis in the tumor cell.

Hormones, metabolites and cytokines released by the microenvironment regulate gene expression to increase glucose uptake and glycolysis in the tumor cell.

cGAS‐STING cellular signaling pathway is activated upon recognition of double‐stranded DNA in the cytosol. cGAS in turn activates the STING protein on the ER to initiate downstream signaling, primarily through TBK‐1 and IKK. STING activation typically leads to the activation of transcription factors, IRF3 and NF‐κB1, which is known to partially inhibit the activity of NF‐κB1.

STING signaling results in the production of IFN‐I and TNF‐α proinflammatory cytokines. Siglec‐sialic (sialidase) axes signaling to represent siglecs on the surface of immune cells and binding with sialic on tumor cell leads to the deactivation of immune response by all the immune cell population as siglec express on most of the immune cell (e.g., T‐cell, TAM, MDSC, NK and neutrophils). Created with BioRender.com Abbreviations: cGAS: cyclic GMP–AMP synthase; STING: stimulator of interferon genes; ER: Endoplasmic Reticulum; TBK‐1: TANK‐binding kinase 1; IKK: nuclear factor‐κB (IκB) kinase; IRF3: Interferon regulatory factor 3; NF‐κB1: nuclear factor κB1; IFN‐I: Type I interferons; TNF‐α: Tumour necrosis factor α; TAM: Tumor‐Associated Macrophage; MDSC: Myeloid‐derived suppressor cell; NK: Natural Killer, TRAF: Tumor‐necrosis factor Receptor‐Associated Factor, TAK: TGF‐β‐activated kinase.

TUMOR MICROENVIRONMENT COMPONENTS

Cellular Components

  • Cancer Cells: The primary malignant cells that proliferate uncontrollably.
  • Stromal Cells: Includes fibroblasts, endothelial cells, and immune cells that support tumor growth and survival.
  • Immune Cells: Comprise various types such as T cells, B cells, macrophages, and natural killer (NK) cells, which can exhibit both pro-tumor and anti-tumor effects depending on their activation state.

Non-Cellular Components

  • Extracellular Matrix (ECM): A network of proteins and carbohydrates that provides structural support to tissues. It is involved in signaling pathways that regulate tumor growth and metastasis.
  • Signaling Molecules: Cytokines and growth factors secreted by tumor and stromal cells that facilitate communication within the TME.

ADAPTIVE IMMUNITY: THE SECOND LINE OF DEFENSE IN FIGHTING FUNGAL PATHOGENS

Key signaling pathways in the TME:

  • Transforming Growth Factor Beta (TGF-β) Signaling: influencing cell proliferation, differentiation, and immune responses. In early tumorigenesis, TGF-β acts as a tumor suppressor; however, in established tumors, it promotes epithelial-mesenchymal transition (EMT), aiding metastasis and immune evasion.
  • Notch Signaling: plays a critical role in cell fate determination and maintaining the balance between tumor-promoting and suppressing signals within the TME.
  • Cytokine and Chemokine Signaling: The TME is rich in cytokines and chemokines that mediate immune cell recruitment and activation. For instance, chemokines such as CCL2 and CCL5 facilitate the infiltration of immune cells like macrophages and T cells, which can have both pro-tumorigenic and anti-tumorigenic effects.
  • Protein Kinase C (PKC) Signaling: PKC signaling can enhance tumor cell survival and promote angiogenesis through the secretion of vascular endothelial growth factor (VEGF).
  • Metabolic Reprogramming: Pathways such as glycolysis are upregulated in response to hypoxic conditions within the TME, leading to increased lactate production that can further modulate immune responses.
  • cGAS-STING Pathway: The cyclic GMP-AMP synthase (cGAS) and stimulator of interferon genes (STING) pathway plays a pivotal role in sensing cytosolic DNA from damaged or stressed cells within the TME. Activation of this pathway leads to type I interferon production, which can enhance anti-tumor immunity.

DYNAMICS OF CANCER MICROENVIRONMENT 

The TME is not a static entity; it undergoes continuous changes influenced by tumor cell behavior. Tumors can manipulate their microenvironment through:

  • Angiogenesis: The formation of new blood vessels to supply nutrients and oxygen to the tumor.
  • Immune Evasion: Tumors can create an immunosuppressive environment that inhibits effective immune responses against them.
  • Metabolic Alterations: Tumors induce changes in local metabolism to adapt to hypoxic (low oxygen) conditions, promoting further growth and invasion.

THERAPEUTIC APPLICATIONS

Understanding the TME opens avenues for targeted therapies:

  • Targeting CAFs: Strategies aimed at inhibiting CAF activity may disrupt tumor progression.
  • Modulating Immune Responses: Immunotherapies that enhance anti-tumor immunity or reprogram immune cells could improve treatment efficacy.
  • Nanomedicine: Developing nanoparticles that can penetrate the dense stroma may enhance drug delivery to tumors.

Targeting signaling pathways like PI3K/AKT, MAPK/ERK, and HIF disrupts tumor support systems, while immunotherapies and TAM/MDSC targeting boost anti-tumor responses in the microenvironment.

(1) Baghban R, et al. Tumor microenvironment complexity and therapeutic implications at a glance. Cell Commun Signal. (2020)7;18(1):59.
(2) Anderson NM, Simon MC. Tumor Microenvironment. Curr Biol. (2020)17;30(16):R921–R925.
(3) Baghban R, et al. Tumor Microenvironment. Medicina (Kaunas). (2019)30;56(1):15.
(4) Goenka A, et al. Tumor microenvironment signaling and therapeutics in cancer progression. Cancer Commun (Lond). (2023);43(5):525-561.

TUMOR MICROENVIRONMENT BIOMARKER LIST

Customize your own signaling pathways (SignArrays®) with the factors of your choice!
Simply download and complete our Personalized SignArrays® information file and send it at [email protected] to get started on your project.

You can check the biomarker list included in this pathway, see below :

Species : Homo sapiens (human)

Human signaling pathways

Signaling PathwaysProduct refInformations

Tumor Microenvironment

TME1H1

List infos


Species : Mus musculus (mouse)

Mouse signaling pathways

Signaling PathwaysProduct refInformations

Tumor Microenvironment

*******

List In progress...


Species : Rattus norvegicus (rat)

Rat signaling pathways

Signaling PathwaysProduct refInformations

Tumor Microenvironment

*******

List In progress...


Species : Sus Scrofa (Pig)

Pig Tumor Microenvironment

Signaling PathwaysProduct refInformations

Tumor Microenvironment

*******

List In progress...


For more information on prices, please click here