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Chromatin modifier MTA1 regulates mitotic transition and tumorigenesis by orchestrating mitotic mRNA processing

Jian Liu1,2, Chunxiao Li1,3, Jinsong Wang1

  • 1State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.

Nature Communications
|September 9, 2020
PubMed

Insights

Cancer metastasis-associated antigen 1 (MTA1) drives cancer by altering RNA splicing during mitosis. MTA1 regulates mitosis genes, causing defective cell division and chromosomal instability, promoting tumor growth.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • Alternative splicing (AS) dysregulation in mitosis is a key driver of cancer.
  • The role of oncogenic chromatin modifiers in cancer-related AS is not well understood.

Purpose of the Study:

  • To investigate the role of cancer metastasis-associated antigen 1 (MTA1) in regulating alternative splicing during mitosis in cancer.
  • To elucidate the molecular mechanisms by which MTA1 influences mitosis and tumorigenesis.

Main Methods:

  • Utilized developed fCLIP-seq technology to identify MTA1-bound transcripts.
  • Investigated the impact of MTA1 deletion on alternative splicing patterns of mitosis regulators.
  • Assessed effects of MTA1 dysfunction on mitotic arrest, chromosome segregation, and chromosomal instability (CIN).

Main Results:

  • MTA1 broadly interacts with and co-expresses with RNA-binding proteins (RBPs) across cancers, influencing mitosis-related AS.
  • MTA1 binds to abundant transcripts at splicing motifs, regulating mRNA levels and AS patterns.
  • MTA1 deletion disrupts dynamic AS switches of ATRX and MYBL2 during mitosis, leading to defective mitotic arrest, aberrant chromosome segregation, and CIN.

Conclusions:

  • MTA1 is a critical regulator of dynamic RNA splicing during mitosis in tumorigenesis.
  • MTA1 orchestrates the splicing of mitosis regulators, contributing to chromosomal instability and cancer progression.
  • Understanding MTA1's role in splicing opens new avenues for cancer therapy targeting mitotic dysregulation.

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