Related Experiment Video

Updated: Oct 5, 2025

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

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

Published on: August 2, 2024

TRIM32 promotes radioresistance by disrupting TC45-STAT3 interaction in triple-negative breast cancer

Yan Ma¹, Haibo Zhang², Cheng Chen³

¹Department of Radiation Oncology, The First Hospital of Lanzhou University, Lanzhou University, Lanzhou, Gansu, 730000, P.R. China.

|January 29, 2022

Abstract:

Radioresistance is common in the treatment of triple-negative breast cancer (TNBC), but the molecular mechanisms involved remain unclear. Herein, we reveal that tripartite motif-containing protein 32 (TRIM32) is upregulated in TNBC and is negatively associated with survival of TNBC patients. Radiotherapy resulted in enhanced expression of TRIM32, whereas TRIM32 depletion reduced TNBC radioresistance in vitro and in vivo. Mechanistically, radiotherapy promoted the association between TRIM32 and nuclear STAT3, which suppressed TC45-induced dephosphorylation of STAT3, resulting in increased STAT3 transcriptional activation and TNBC radioresistance. Finally, we demonstrated that TRIM32 and STAT3 phosphorylation are co-expressed in TNBC tissues. Moreover, high expression of TRIM32 and STAT3 phosphorylation is positively linked to poor prognosis of TNBC patients. Our study demonstrates that TRIM32 is a novel target for predicting radioresistance in TNBC patients.

Insights

Tripartite motif-containing protein 32 (TRIM32) promotes radioresistance in triple-negative breast cancer (TNBC) by enhancing STAT3 activation. Targeting TRIM32 may improve TNBC treatment outcomes and predict patient survival.

Area of Science:

Oncology
Molecular Biology
Cancer Research

Background:

Radioresistance is a significant challenge in treating triple-negative breast cancer (TNBC).
The underlying molecular mechanisms contributing to TNBC radioresistance are not fully understood.
Identifying novel therapeutic targets is crucial for improving patient outcomes.

Purpose of the Study:

To investigate the role of tripartite motif-containing protein 32 (TRIM32) in TNBC radioresistance.
To elucidate the molecular mechanisms by which TRIM32 influences radioresistance.
To evaluate TRIM32 as a potential predictive biomarker for TNBC radioresistance.

Main Methods:

Analysis of TRIM32 expression in TNBC tissues and its correlation with patient survival.
In vitro and in vivo experiments assessing the impact of TRIM32 depletion on TNBC radioresistance.
Investigation of the interaction between TRIM32, STAT3, and TC45 following radiotherapy.
Assessment of TRIM32 and STAT3 phosphorylation co-expression in TNBC patient tissues.

Main Results:

TRIM32 is upregulated in TNBC and associated with poor patient survival.
Radiotherapy enhances TRIM32 expression, while TRIM32 depletion reduces TNBC radioresistance.
TRIM32 promotes TNBC radioresistance by enhancing STAT3 transcriptional activation via suppression of STAT3 dephosphorylation.
Co-expression of TRIM32 and phosphorylated STAT3 correlates with poor prognosis in TNBC patients.

Conclusions:

TRIM32 plays a critical role in promoting radioresistance in triple-negative breast cancer.
TRIM32 enhances radioresistance by modulating the TRIM32-STAT3 signaling pathway.
TRIM32 serves as a novel predictive biomarker for radioresistance and prognosis in TNBC.

Read full analysis

More Related Videos

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model

Published on: March 20, 2020

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Related Concept Videos

Targeted Cancer Therapies

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...

mTOR Signaling and Cancer Progression

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...

Articles linked to this work by shared authors, journal, and citation graph.

Distinct immune cell dynamics associated with immune-related adverse events during combined chemoradiation and immune checkpoint inhibitor therapy.

Nature communications·2025

KMT5A-methylated SNIP1 promotes triple-negative breast cancer metastasis by activating YAP signaling.

Nature communications·2022

Heparin-binding growth factor (HDGF) drives radioresistance in breast cancer by activating the STAT3 signaling pathway.

Journal of translational medicine·2021

Tripartite motif containing 24 regulates cell proliferation in colorectal cancer through YAP signaling.

Cancer medicine·2020

Betulinic acid ameliorates experimental diabetic-induced renal inflammation and fibrosis via inhibiting the activation of NF-κB signaling pathway.

Molecular and cellular endocrinology·2016

Investigating polymorphisms by bioinformatics is a potential cost-effective method to screen for germline mutations in Chinese familial adenomatous polyposis patients.

Oncology letters·2016

See all related articles