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NF-κB-dependent Signaling Pathway

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Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
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Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Mechanism of miR-7 mediating TLR4/TRAF6/NF-κB inflammatory pathway in colorectal cancer.

Jianfeng Ren1, Bing Han1, Ping Feng1

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Functional & Integrative Genomics
|February 5, 2024
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Summary

MicroRNA-7 (miR-7) is underexpressed in colorectal cancer (CRC), while Toll-like receptor 4 (TLR4) is increased. Restoring miR-7 inhibits CRC progression by targeting the TLR4/TRAF6/NF-κB pathway, suggesting miR-7 as a potential biomarker.

Keywords:
NF-κB, Colorectal cancerTRAF6miR-7, TLR4

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Area of Science:

  • Molecular Biology
  • Oncology
  • Immunology

Background:

  • Colorectal cancer (CRC) progression involves complex molecular mechanisms.
  • Toll-like receptor 4 (TLR4) and microRNA-7 (miR-7) are implicated in various cancers.
  • Understanding their interplay is crucial for developing novel therapeutic strategies.

Purpose of the Study:

  • To investigate the roles of TLR4 and miR-7 in colorectal cancer (CRC) development.
  • To elucidate the regulatory relationship between miR-7 and TLR4.
  • To explore the underlying signaling pathways involved in CRC progression.

Main Methods:

  • Quantitative reverse transcription-polymerase chain reaction (RT-qPCR) for gene expression analysis.
  • Dual luciferase reporter assays to confirm miR-7 targeting of TLR4.
  • In vitro assays (MTT, wound healing, invasion) to assess cell behavior.
  • Western blotting to analyze the TRAF6/NF-κB signaling pathway.

Main Results:

  • miR-7 was significantly underexpressed in CRC tissues and cells, whereas TLR4 expression was upregulated.
  • miR-7 directly inhibited TLR4 expression, and its restoration suppressed CRC cell proliferation, migration, and invasion.
  • TLR4 knockdown exhibited opposing effects, inhibiting CRC cell growth and metastasis.
  • The TRAF6/NF-κB signaling pathway was identified as a key mediator of TLR4's pro-tumorigenic effects.

Conclusions:

  • miR-7 acts as a tumor suppressor in CRC by negatively regulating TLR4 and inhibiting the TRAF6/NF-κB pathway.
  • Restoring miR-7 expression may represent a promising therapeutic approach for CRC.
  • miR-7 demonstrates potential as a sensitive biomarker for CRC diagnosis and prognosis.