Related Experiment Video

Updated: May 8, 2026

Real-time Imaging of Myeloid Cells Dynamics in ApcMin/+ Intestinal Tumors by Spinning Disk Confocal Microscopy
05:21

Real-time Imaging of Myeloid Cells Dynamics in ApcMin/+ Intestinal Tumors by Spinning Disk Confocal Microscopy

Published on: October 6, 2014

CKIP-1 acts as a colonic tumor suppressor by repressing oncogenic Smurf1 synthesis and promoting Smurf1

J Nie1, L Liu2, G Xing3

  • 11] Department of Molecular Biology, Institute of Basic Medicine, PLA General Hospital, Beijing, China [2] State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing, China.

Oncogene
|September 3, 2013
PubMed

Insights

Casein kinase-2 interacting protein-1 (CKIP-1) acts as a tumor suppressor in colon cancer by downregulating the oncogene Smurf1. CKIP-1 downregulation promotes colon cancer progression through the PI3K/Akt/mTOR pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Cellular signaling pathway dysregulation is implicated in colon cancer development.
  • Key regulators of colon carcinogenesis remain underexplored.
  • Casein kinase-2 interacting protein-1 (CKIP-1) is known for its role in bone formation.

Purpose of the Study:

  • To investigate the role of CKIP-1 in colon cancer.
  • To elucidate the molecular mechanisms underlying CKIP-1's function in colon carcinogenesis.
  • To explore the relationship between CKIP-1 and Smad ubiquitylation regulatory factor-1 (Smurf1) in colon cancer.

Main Methods:

  • Analysis of CKIP-1 expression in human colon cancer tissues and cell lines.
  • CKIP-1 silencing and overexpression experiments in colon cancer cell lines (HCT116, SW480).
  • In vivo tumor formation assays.
  • Investigation of the phosphatidylinositol-3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway and Smurf1 regulation.

Main Results:

  • CKIP-1 was downregulated in colon cancer tissues and cell lines, correlating with progression.
  • CKIP-1 overexpression inhibited colon cancer cell growth, migration, and in vivo tumor formation.
  • CKIP-1 suppressed colon cancer by downregulating Smurf1 via inhibition of PI3K/Akt/mTOR signaling and enhanced Smurf1 degradation.
  • CKIP-1 silencing was associated with promoter methylation.

Conclusions:

  • CKIP-1 functions as a tumor suppressor in colon cancer.
  • CKIP-1 downregulation contributes to colon carcinogenesis by upregulating Smurf1.
  • The CKIP-1/Smurf1 axis, modulated by PI3K/Akt/mTOR signaling, represents a novel mechanism in colon cancer.

More Related Videos

Protocols for Analyzing the Role of Paneth Cells in Regenerating the Murine Intestine using Conditional Cre-lox Mouse Models07:48

Protocols for Analyzing the Role of Paneth Cells in Regenerating the Murine Intestine using Conditional Cre-lox Mouse Models

Published on: November 21, 2015

In vitro Organoid Culture of Primary Mouse Colon Tumors07:33

In vitro Organoid Culture of Primary Mouse Colon Tumors

Published on: May 17, 2013

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...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic cells are...