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Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

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 daughter...
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Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
Separation of Sister Chromatids02:17

Separation of Sister Chromatids

At the transition from prophase to metaphase, there is a reduction in cohesion along the chromosomal arms, resulting in the resolution of sister chromatids. However, residual cohesin connections remain to hold the sister chromatids together until the transition from metaphase to anaphase. The residual connection prevents any premature separation of sister chromatids, blocking the risks of aneuploidy within the daughter cells.
At the onset of anaphase, separase, a proteolytic enzyme, is...
Regulation of Nuclear Protein Sorting01:45

Regulation of Nuclear Protein Sorting

Nuclear protein sorting regulates nucleus composition and gene expression, crucial for determining the fate of a eukaryotic cell. Hence, the entry and exit of molecules across the nuclear envelope is a tightly controlled process. Nuclear protein sorting can be inhibited by one of the following ways: 1) masking cargo signal sequences, 2) modifying the nuclear receptor's affinity for cargo, 3) controlling the nuclear pore size, 4) retaining the cargo during its transit to the cytosol or the...
Cell Specific Gene Expression01:58

Cell Specific Gene Expression

Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...

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Updated: May 31, 2026

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
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Published on: July 28, 2010

SREBP2-activated CNPY3 Phase Separation Promotes Colorectal Cancer by Enhancing MDM2-mediated p53 Degradation.

Xue Li1,2, Min-Yue Yin1, Yan-Fei Wei1

  • 1Department of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory of Digestive Health, National Clinical Research Center for Digestive Diseases, Beijing Key Laboratory for Precancerous Lesion of Digestive Diseases, Beijing, 100050, China.

International Journal of Biological Sciences
|May 29, 2026
PubMed
Summary

Dysregulated cholesterol metabolism fuels colorectal cancer (CRC) via SREBP2-activated CNPY3. This protein targets wild-type p53, promoting tumor growth. CNPY3 is a potential biomarker and therapeutic target for CRC.

Keywords:
CNPY3Cholesterol MetabolismColorectal CancerLiquid-liquid phase seperationMDM2SREBP2

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Analysis of SCAP N-glycosylation and Trafficking in Human Cells
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Analysis of SCAP N-glycosylation and Trafficking in Human Cells

Published on: November 8, 2016

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Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
28:15

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Published on: July 28, 2010

Analysis of SCAP N-glycosylation and Trafficking in Human Cells
11:27

Analysis of SCAP N-glycosylation and Trafficking in Human Cells

Published on: November 8, 2016

Area of Science:

  • Oncology
  • Molecular Biology
  • Metabolic Pathways

Background:

  • Cholesterol metabolism is a key hallmark of cancer.
  • The transcription factor SREBP2 regulates cholesterol synthesis but its role in colorectal cancer (CRC) oncogenesis is unclear.
  • Understanding how metabolic dysregulation drives CRC is crucial for developing new therapies.

Purpose of the Study:

  • To investigate the role of SREBP2-mediated cholesterol metabolism in colorectal cancer.
  • To identify downstream targets of SREBP2 in CRC and elucidate their function.
  • To explore the potential of CNPY3 as a prognostic biomarker and therapeutic target in CRC.

Main Methods:

  • Clinical and preclinical analyses of hypercholesterolemia and SREBP2 levels in CRC.
  • Multi-omics integration to identify SREBP2 transcriptional targets.
  • Functional assays assessing CNPY3's role in CRC cell proliferation, invasion, and tumor growth.
  • Mechanistic studies involving liquid-liquid phase separation (LLPS), MDM2 phosphorylation, p53 degradation, and Nutlin-3 treatment.

Main Results:

  • Hypercholesterolemia and elevated tumoral SREBP2 are confirmed hallmarks of CRC.
  • CNPY3 is identified as a direct SREBP2 target, driving CRC progression independently of cholesterol synthesis.
  • CNPY3 utilizes liquid-liquid phase separation (LLPS) to promote MDM2-mediated degradation of wild-type p53, enhancing tumor growth.
  • High CNPY3 expression correlates with advanced disease and poor patient survival.

Conclusions:

  • A novel SREBP2-CNPY3-MDM2-p53 signaling axis links cholesterol dysregulation to p53 inactivation in CRC.
  • CNPY3's oncogenic function is mediated by its LLPS property, specifically targeting wild-type p53.
  • CNPY3 represents a promising prognostic biomarker and therapeutic target for p53-wild-type colorectal cancer.