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Long Non-Coding RNA SPRY4-IT1 Reverses Cisplatin Resistance by Downregulating MPZL-1 via Suppressing EMT in NSCLC

Yunyao Ye1,2, Jingyao Gu1, Pei Liu1,3

  • 1Department of Oncology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, People's Republic of China.

Oncotargets and Therapy
|April 21, 2020
PubMed
Abstract

Insights

Long non-coding RNA SPRY4 intronic transcript 1 (SPRY4-IT1) can reverse cisplatin resistance in non-small-cell lung cancer (NSCLC). Upregulating SPRY4-IT1 inhibits tumor growth and metastasis by downregulating MPZL-1 and suppressing epithelial-mesenchymal transition (EMT).

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer development.
  • SPRY4 intronic transcript 1 (SPRY4-IT1) has been implicated in various tumor types.
  • The specific function of SPRY4-IT1 in cisplatin resistance in non-small-cell lung cancer (NSCLC) is not well understood.

Purpose of the Study:

  • To investigate the role and molecular mechanisms of SPRY4-IT1 in cisplatin resistance in NSCLC.
  • To determine if SPRY4-IT1 affects cell proliferation, apoptosis, and epithelial-mesenchymal transition (EMT) in cisplatin-resistant NSCLC cells.

Main Methods:

  • Quantitative real-time polymerase chain reaction (RT-qPCR) and Western blotting were used to assess gene and protein expression.
  • Cell counting kit-8 (CCK8), colony formation assays, and flow cytometry evaluated proliferation and apoptosis.
  • In vivo studies involved injecting transfected cells into nude mice to assess cisplatin resistance.
  • Microarray analysis identified potential SPRY4-IT1 targets.

Main Results:

  • SPRY4-IT1 expression was significantly decreased in cisplatin-resistant NSCLC cells (A549/DDP) compared to parental cells.
  • Overexpression of SPRY4-IT1 suppressed proliferation and induced apoptosis in A549/DDP cells, both in vitro and in vivo.
  • SPRY4-IT1 negatively regulated MPZL-1 expression.
  • Upregulation of SPRY4-IT1 and downregulation of MPZL-1 inhibited EMT, evidenced by increased E-cadherin and decreased Vimentin.

Conclusions:

  • SPRY4-IT1 upregulation can reverse the cisplatin-resistant phenotype in NSCLC.
  • This reversal is partly mediated by the downregulation of MPZL-1, which in turn inhibits the EMT process.
  • SPRY4-IT1 serves as a potential therapeutic target for overcoming cisplatin resistance in NSCLC.
Keywords:
EMTMPZL-1SPRY4-IT1cisplatin resistancelong non-coding RNA

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