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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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Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...

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Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
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NOP56 Drives Colorectal Cancer Progression by Modulating p53 Acetylation through SIRT1/p300.

Ji Eon Park1, Chi-Hoon Ahn1, Deok Yong Sim1

  • 1Cancer Molecular Targeted Herbal Research Laboratory, College of Korean Medicine, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul 02447, South Korea.

International Journal of Biological Sciences
|May 20, 2026
PubMed
Summary

Nucleolar protein 56 (NOP56) drives colorectal cancer (CRC) by degrading p53. Inhibiting NOP56 triggers apoptosis via p53 acetylation, offering a new therapeutic target for p53 wild-type CRC.

Keywords:
NOP56SIRT1apoptosiscolorectal cancerp300p53 acetylation

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Area of Science:

  • Oncology
  • Molecular Biology

Background:

  • Nucleolar protein 56 (NOP56) is involved in oncogenesis via reactive oxygen species (ROS) homeostasis.
  • The specific role of NOP56 in colorectal cancer (CRC) progression is not well understood.

Purpose of the Study:

  • To investigate the clinical significance and biological function of NOP56 in colorectal cancer (CRC).
  • To explore NOP56 as a potential therapeutic target for CRC.

Main Methods:

  • Analysis of TCGA datasets and tissue microarrays.
  • Next-generation sequencing, in vitro and in vivo experimental models.
  • Investigation of NOP56's impact on cell viability, migration, apoptosis, and p53 pathway modulation.

Main Results:

  • NOP56 expression is elevated in CRC tissues and linked to poor survival.
  • NOP56 silencing suppresses CRC cell growth, migration, and induces apoptosis and cell cycle arrest.
  • NOP56 promotes p53 degradation; its inhibition enhances p53 stability and acetylation via the SIRT1/p300 axis.
  • NOP56 knockdown synergizes with 5-fluorouracil (5-FU) and reduces tumor growth in vivo.

Conclusions:

  • NOP56 acts as an oncogenic driver in CRC by promoting p53 degradation.
  • Inhibition of NOP56 induces apoptosis through p53 acetylation, regulated by the SIRT1/p300 pathway.
  • NOP56 is identified as a promising therapeutic target for p53 wild-type colorectal cancer.