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Related Concept Videos

The Ras Gene02:38

The Ras Gene

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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
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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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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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Small GTPases - Ras and Rho01:24

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Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
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M-Cdk Drives Transition Into Mitosis02:15

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Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
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Abnormal Proliferation02:23

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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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RhoC GTPase Activation Assay
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CSDE1 Drives Glycolysis and the Progression of Prostate Cancer Through RAC1-Dependent RAS/MAPK Activation.

Zhen Yin1, Zefeng Wang1, Wei Gong1

  • 1Department of Urology, Renmin Hospital of Wuhan University, Wuhan, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|March 11, 2026
PubMed
Summary
This summary is machine-generated.

The study found that CSDE1 promotes prostate cancer (PCa) growth by enhancing RAC1 signaling and metabolism. Lowering CSDE1 levels may offer a new therapeutic strategy for PCa patients.

Keywords:
CSDE1RAC1RAS/MAPKbiomarkerglycolysisprostate cancer

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Prostate cancer (PCa) is a major cause of male cancer mortality.
  • Identifying molecular drivers of PCa progression is crucial for developing new treatments.

Purpose of the Study:

  • To investigate the role of CSDE1 in prostate cancer progression.
  • To elucidate the molecular mechanisms underlying CSDE1's function in PCa.

Main Methods:

  • Analysis of CSDE1 expression in PCa tissues.
  • In vitro studies involving CSDE1 knockdown in PCa cells.
  • Assessment of cell proliferation, migration, invasion, and metabolic activity (ECAR, OCR, lactate).
  • Investigation of CSDE1's association with RAC1, MAPK signaling, GLUT1, and LDHA.
  • In vivo tumor growth models.

Main Results:

  • CSDE1 was upregulated in PCa and linked to poorer survival in high Gleason score patients.
  • CSDE1 knockdown inhibited PCa cell proliferation, migration, invasion, and suppressed metabolic activity.
  • CSDE1 expression correlated with RAC1, MAPK pathway alterations, GLUT1, and LDHA.
  • The CSDE1-RAC1 axis was validated in vivo as promoting tumor growth.

Conclusions:

  • CSDE1 drives PCa progression by activating RAC1-mediated MAPK signaling and altering cellular metabolism.
  • CSDE1 represents a potential prognostic biomarker and therapeutic target for prostate cancer.