Related Experiment Video
Updated: Jul 31, 2025

Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells
Published on: April 26, 2017
TRA2: The dominant power of alternative splicing in tumors
Jiancheng Xue1,2, Tie Ma3, Xiaowen Zhang1,2
1Medical Research Center, Shengjing Hospital of China Medical University, Shenyang, China.
Abstract:
The dysregulation of alternative splicing (AS) is frequently found in cancer and considered as key markers for cancer progression and therapy. Transformer 2 (TRA2), a nuclear RNA binding protein, consists of transformer 2 alpha homolog (TRA2A) and transformer 2 beta homolog (TRA2B), and plays a role in the regulation of pre-mRNA splicing. Growing evidence has been provided that TRA2A and TRA2B are dysregulated in several types of tumors, and participate in the regulation of proliferation, migration, invasion, and chemotherapy resistance in cancer cells through alteration of AS of cancer-related genes. In this review, we highlight the role of TRA2 in tumorigenesis and metastasis, and discuss potential molecular mechanisms how TRA2 influences tumorigenesis and metastasis via controlling AS of pre-mRNA. We propose that TRA2Ais a novel biomarker and therapeutic target for cancer progression and therapy.
Insights
Alternative splicing (AS) dysregulation in cancer involves Transformer 2 (TRA2) proteins. TRA2A and TRA2B impact tumor progression and therapy by altering AS, with TRA2A emerging as a potential cancer biomarker and therapeutic target.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Alternative splicing (AS) is frequently dysregulated in cancer, serving as a marker for disease progression and therapeutic response.
- Transformer 2 (TRA2) proteins, including TRA2A and TRA2B, are nuclear RNA-binding proteins crucial for regulating pre-mRNA splicing.
- Evidence indicates TRA2A and TRA2B are dysregulated in various tumors, influencing cancer cell proliferation, migration, invasion, and chemotherapy resistance.
Purpose of the Study:
- To review the role of TRA2 proteins in tumorigenesis and metastasis.
- To discuss the molecular mechanisms by which TRA2 influences cancer development and spread through AS control.
- To identify TRA2A as a potential biomarker and therapeutic target for cancer.
Main Methods:
- Literature review focusing on the role of TRA2 proteins in cancer.
- Analysis of existing evidence on TRA2-mediated alternative splicing in cancer-related genes.
- Discussion of molecular pathways linking TRA2, AS, and cancer progression.
Main Results:
- TRA2 proteins (TRA2A and TRA2B) are implicated in the regulation of key cancer hallmarks, including proliferation, migration, and invasion.
- Dysregulation of TRA2A and TRA2B contributes to chemotherapy resistance in cancer cells via altered AS.
- TRA2 proteins influence tumorigenesis and metastasis by controlling the alternative splicing of oncogenic and tumor-suppressor genes.
Conclusions:
- TRA2 proteins play a significant role in cancer progression and metastasis through the modulation of alternative splicing.
- TRA2A is highlighted as a promising novel biomarker for cancer progression.
- TRA2A represents a potential therapeutic target for improving cancer therapy outcomes.
Related Concept Videos
RNA Splicing
Alternative RNA Splicing
There are five types of alternative RNA splicing that vary in the ways the pre-mRNA segments are removed or retained in the mature mRNA. The first...
Abnormal Proliferation
Cancer-Critical Genes II: Tumor Suppressor Genes
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 Functions
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...
Cancers Originate from Somatic Mutations in a Single Cell

