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Long noncoding RNA MALAT1 affects the efficacy of radiotherapy for esophageal squamous cell carcinoma by regulating

Zhijun Li1, Yang Zhou1, Bo Tu1

  • 1Department of Radiation Oncology, Inner Mongolia Autonomous Region Peoples Hospital, Hohhot, China.

Journal of Oral Pathology & Medicine : Official Publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
|December 10, 2016
PubMed
Abstract

Insights

Long noncoding RNA MALAT1 promotes radioresistance in esophageal squamous cell carcinoma by upregulating Cks1. Targeting MALAT1 may enhance radiotherapy effectiveness for ESCC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is implicated in various cancers.
  • The role of MALAT1 in tumor radioresistance, particularly in esophageal cancer, remains unclear.
  • Understanding MALAT1's function is crucial for improving esophageal squamous cell carcinoma (ESCC) treatment.

Purpose of the Study:

  • To investigate the role of MALAT1 in regulating radiosensitivity in esophageal cancer (EC), specifically ESCC.
  • To explore the underlying mechanism involving Cks1 expression.
  • To assess the therapeutic potential of targeting MALAT1 in ESCC.

Main Methods:

  • Establishment of ESCC xenografts in nude mice.
  • Quantitative real-time PCR and Western blot to assess MALAT1 and Cks1 expression.
  • In vitro functional assays using cell transfection with plasmids or siRNAs for MALAT1 and Cks1.
  • Evaluation of cell viability (MTT assay) and apoptosis (TUNEL assay) after irradiation.

Main Results:

  • Both MALAT1 and Cks1 expression decreased upon irradiation in xenografts and cells.
  • Overexpression of MALAT1 enhanced radioresistance by inhibiting irradiation-induced apoptosis and promoting cell viability, while downregulating Cks1.
  • MALAT1 siRNA reduced radioresistance, and Cks1 siRNA reversed MALAT1-induced radioresistance.
  • Tumor growth was enhanced with MALAT1 overexpression, along with Cks1 upregulation, especially under radiation.

Conclusions:

  • MALAT1 positively regulates radioresistance in ESCC, partly by promoting Cks1 expression.
  • Targeting MALAT1 presents a promising strategy to enhance the efficacy of radiotherapy for ESCC.
Keywords:
Cks1MALAT1esophageal squamous cell carcinomaradioresistance

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