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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.
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Updated: Jun 19, 2026

Exploring the Pharmacological Action and Molecular Mechanism of Salidroside in Inhibiting MCF-7 Cell Proliferation and Migration
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Published on: June 9, 2023

RBM38 Regulates HORMAD1 Splicing to Enhances MEK Inhibitor Sensitivity in Breast Cancer.

Chenyan Sun1, Huacheng Luo1, Jing Zhang2

  • 1Chinese Academy of Sciences Hangzhou Institute of Medicine.

RNA (New York, N.Y.)
|June 17, 2026
PubMed
Summary
This summary is machine-generated.

BRCA1-mutant breast cancers develop resistance to PARP inhibitors. This study identifies a new vulnerability involving HORMAD1 regulation by RBM38, suggesting splicing modulation as a novel therapeutic strategy.

Keywords:
BRCA1; HORMAD1; alternative splicing; RBM38; MEK inhibitor

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Using RNA-sequencing to Detect Novel Splice Variants Related to Drug Resistance in In Vitro Cancer Models
09:58

Using RNA-sequencing to Detect Novel Splice Variants Related to Drug Resistance in In Vitro Cancer Models

Published on: December 9, 2016

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Mutations in BRCA1 impair homologous recombination, driving breast cancer.
  • BRCA1-deficient tumors often develop resistance to PARP inhibitors, necessitating new therapeutic targets.
  • HORMAD1 overexpression in triple-negative breast cancer is linked to genomic instability, but its role in therapy response is unknown.

Purpose of the Study:

  • To investigate the role of HORMAD1 in BRCA1-mutant breast cancer therapy response.
  • To identify molecular vulnerabilities in BRCA1-deficient tumors resistant to standard treatments.
  • To explore the potential of targeting splicing regulation for enhancing treatment efficacy.

Main Methods:

  • Transcriptomic profiling of BRCA1-mutant breast cancer.
  • Treatment with splicing inhibitor Isoginkgetin.
  • Analysis of RNA-binding protein RBM38 and HORMAD1 splicing.
  • Assessment of MEK1 inhibition sensitivity after RBM38 knockdown.

Main Results:

  • HORMAD1 was identified as a highly upregulated and alternatively spliced gene in BRCA1-mutant breast cancer.
  • Isoginkgetin promoted HORMAD1 exon 4 inclusion, altering splicing patterns.
  • RBM38 knockdown sensitized BRCA1-mutant cells to MEK1 inhibition, highlighting an RBM38-HORMAD1 axis.
  • Splicing regulation emerged as a potential therapeutic vulnerability.

Conclusions:

  • The RBM38-HORMAD1 signaling pathway represents a potential therapeutic vulnerability in BRCA1-mutant breast cancer.
  • Targeting splicing regulation offers a promising strategy to overcome resistance and enhance treatment efficacy.
  • Further research into splicing modulation could lead to novel therapeutic approaches for breast cancer treatment.