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Related Concept Videos

The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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MAPK Signaling Cascades01:07

MAPK Signaling Cascades

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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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mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
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Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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Abnormal Proliferation02:23

Abnormal Proliferation

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Cancer Cell Migration through Invadopodia01:35

Cancer Cell Migration through Invadopodia

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Invadosome is a broad category of cell surface structures with proteolytic activity that  degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However,...
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Related Experiment Video

Updated: May 31, 2025

Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
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CDCA4 promotes bladder cancer progression by JAK/STAT signaling pathway.

Peng Wan1, Yuan Ren1, Hao Deng2

  • 1Department of Oncology, The First Affiliated Hospital of Yangtze University, Jingzhou, 434000, China.

Journal of Cancer Research and Clinical Oncology
|January 24, 2025
PubMed
Summary

Cell division cycle associated 4 (CDCA4) promotes bladder cancer progression by activating the JAK/STAT pathway. Inhibiting CDCA4 may offer a new therapeutic strategy for bladder cancer patients.

Keywords:
AG490Bladder cancerCDCA4JAK/STATMolecular target

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An Orthotopic Bladder Cancer Model for Gene Delivery Studies
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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Cell division cycle associated 4 (CDCA4) is involved in tumor progression.
  • Its specific role in bladder cancer pathogenesis is not well understood.

Purpose of the Study:

  • To investigate the role and mechanism of CDCA4 in bladder cancer.
  • To evaluate CDCA4 as a potential therapeutic target.

Main Methods:

  • Analysis of TCGA and GEO bladder cancer datasets for CDCA4 expression and prognosis.
  • In vitro experiments using CDCA4-overexpressing and knockdown bladder cancer cell lines.
  • Assays for cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT).
  • Western blot and pathway analysis to identify downstream targets.

Main Results:

  • CDCA4 expression is upregulated in bladder cancer and linked to poor prognosis.
  • CDCA4 inhibition suppressed bladder cancer cell proliferation, migration, invasion, and EMT.
  • CDCA4 overexpression enhanced bladder cancer cell malignancy.
  • CDCA4 activates the JAK/STAT signaling pathway, promoting bladder cancer progression.

Conclusions:

  • CDCA4 promotes bladder cancer cell proliferation, migration, and invasion via the JAK/STAT pathway.
  • CDCA4 represents a potential novel molecular target for bladder cancer treatment.