Related Experiment Video

Updated: Nov 6, 2025

Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
09:40

Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer

Published on: August 2, 2024

2.9K

TRIM25 regulates oxaliplatin resistance in colorectal cancer by promoting EZH2 stability

Sha Zhou1, Jianhong Peng2, Liuniu Xiao3

  • 1Department of Radiation Oncology, Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, 510060, China.

Cell Death & Disease
|May 9, 2021
PubMed

Insights

This study reveals TRIM25 as a key factor in colorectal cancer (CRC) resistance to oxaliplatin chemotherapy. Targeting TRIM25 may improve treatment outcomes for CRC patients experiencing recurrence.

Area of Science:

  • Oncology
  • Cancer Epigenetics
  • Chemotherapy Resistance

Background:

  • Chemotherapy resistance is a primary obstacle in effective colorectal cancer (CRC) treatment.
  • Oxaliplatin (OXA) is a cornerstone chemotherapy agent for CRC, but resistance limits its efficacy.
  • Understanding the molecular mechanisms underlying OXA resistance is crucial for improving patient survival.

Purpose of the Study:

  • To identify novel epigenetic regulators involved in oxaliplatin resistance in colorectal cancer.
  • To investigate the role of TRIM25 in mediating oxaliplatin resistance and its association with patient outcomes.
  • To elucidate the molecular mechanisms by which TRIM25 influences colorectal cancer cell behavior and drug response.

Main Methods:

  • Analysis of TRIM25 expression levels in colorectal cancer patient cohorts with varying oxaliplatin response.
  • In vitro and in vivo experiments assessing the impact of TRIM25 modulation (downregulation and overexpression) on colorectal cancer cell survival and stemness.
  • Investigation of the interaction between TRIM25, TRAF6, and EZH2 to understand the molecular pathway regulating oxaliplatin resistance.

Main Results:

  • Elevated TRIM25 expression correlates significantly with oxaliplatin resistance, higher recurrence rates, and poorer disease-free survival in colorectal cancer patients.
  • TRIM25 downregulation sensitizes colorectal cancer cells to oxaliplatin, while its overexpression enhances resistance and promotes cancer stem cell properties.
  • TRIM25 functions by inhibiting the interaction between E3 ubiquitin ligase TRAF6 and EZH2, leading to EZH2 stabilization and upregulation, thereby promoting oxaliplatin resistance.

Conclusions:

  • TRIM25 is identified as a critical epigenetic regulator of oxaliplatin resistance in colorectal cancer.
  • TRIM25 promotes colorectal cancer cell survival and stemness, contributing to treatment failure.
  • Targeting TRIM25 presents a promising therapeutic strategy to overcome oxaliplatin resistance in colorectal cancer management.

More Related Videos

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

14.0K
Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres06:52

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres

Published on: July 22, 2020

6.7K

Related Concept Videos

Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.5K
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...
4.8K
Drugs that Stabilize Microtubules01:15

Drugs that Stabilize Microtubules

Microtubules are dynamic structures that undergo cycles of catastrophe and rescue. The microtubules play a central role in cell division by forming the spindle apparatus for segregating the chromosomes. This makes them ideal targets for regulating dividing cells in tumors and malignant cancer cells. Microtubule stabilizing drugs help stabilize the microtubule formation and promote its polymerization. Paclitaxel was the first microtubule stabilizing agent used as anticancer drug in chemotherapy...
2.3K
Drugs that Destabilize Microtubules01:10

Drugs that Destabilize Microtubules

Microtubules are dynamic structures and can be regulated by microtubule targeting agents (MTAs). Microtubule destabilizing drugs are a class of MTAs that destabilize and prevent microtubules' polymerization. Both natural and synthetic chemicals can be found under this class of drugs. Vincristine and vinblastine, two vinca alkaloids, and colchicine were among the first to be discovered. These drugs can affect cells in various ways, either by inducing a change in cell morphology, preventing...
2.2K