Related Experiment Video

Updated: Dec 2, 2025

An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells
08:54

An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells

Published on: July 20, 2014

14.3K

CPEB3 functions as a tumor suppressor in colorectal cancer via JAK/STAT signaling

Yuxin Fang1, Qian Zhong1, Yadong Wang1

  • 1Guangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.

Aging
|November 4, 2020
PubMed

Insights

Cytoplasmic polyadenylation element binding protein 3 (CPEB3) acts as a tumor suppressor in colorectal cancer. Reduced CPEB3 expression promotes cancer cell proliferation and metastasis by activating the JAK/STAT pathway.

Area of Science:

  • Molecular Biology
  • Oncology
  • Gene Regulation

Background:

  • Cytoplasmic polyadenylation element binding proteins (CPEBs) regulate gene expression post-transcriptionally.
  • The specific role of CPEB3 in cancer development, particularly colorectal cancer, remains largely uncharacterized.

Purpose of the Study:

  • To investigate the role and mechanism of CPEB3 in colorectal cancer progression.
  • To determine the clinical significance of CPEB3 expression in colorectal cancer patients.

Main Methods:

  • Analysis of CPEB3 expression in colorectal cancer tissues.
  • In vitro studies assessing the impact of CPEB3 on cancer cell proliferation, migration, and invasion.
  • Mechanistic studies involving RNA binding assays and JAK/STAT pathway analysis.

Main Results:

  • Colorectal cancer tissues showed significantly lower CPEB3 expression compared to normal tissues.
  • Downregulated CPEB3 expression correlated with poorer patient prognosis.
  • Reduced CPEB3 levels enhanced colorectal cancer cell proliferation, migration, and invasion.
  • CPEB3 directly binds to the 3'UTR of JAK1 mRNA, inhibiting the JAK/STAT pathway.
  • CPEB3 knockdown led to increased JAK-STAT signaling and promoted cancer cell metastasis.

Conclusions:

  • CPEB3 functions as a tumor suppressor in colorectal cancer.
  • CPEB3 inhibits colorectal cancer progression by post-transcriptionally regulating the JAK/STAT signaling pathway via JAK1 mRNA binding.
Keywords:
CPEB3metastasispost-transcriptional regulationproliferationtumor suppressor

More Related Videos

A Multiplexed Luciferase-based Screening Platform for Interrogating Cancer-associated Signal Transduction in Cultured Cells10:13

A Multiplexed Luciferase-based Screening Platform for Interrogating Cancer-associated Signal Transduction in Cultured Cells

Published on: July 3, 2013

11.5K
Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies09:29

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies

Published on: September 30, 2016

14.2K

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...
4.9K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

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...
10.7K
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal01:22

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
2.5K
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...
7.0K
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...
2.3K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
4.9K