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Long non-coding RNA terminal differentiation-induced non-coding RNA regulates cisplatin resistance of choroidal

Wei Li1, Aiqin Nie1, Longyu Jin1

  • 1Department of Ophthalmology, The Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen City, Guangdong Province, 518000 P. R. China.

Bioengineered
|January 24, 2022
PubMed

Insights

Long non-coding RNA TINCR promotes cisplatin resistance in choroidal melanoma by regulating the miR-19b-3p/ERK-2/NF-kb pathway. TINCR represents a potential therapeutic target for overcoming cisplatin resistance in choroidal melanoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Choroidal melanoma (CM) exhibits resistance to cisplatin (DDP) chemotherapy.
  • The role of long non-coding RNAs (lncRNAs) in chemoresistance is an emerging area of research.

Purpose of the Study:

  • To investigate the function of TINCR in DDP resistance in CM.
  • To elucidate the underlying molecular mechanisms involving miR-19b-3p, ERK-2, and NF-kb.

Main Methods:

  • Quantitative real-time PCR and Western blot for gene and protein expression analysis.
  • CCK-8 assay, flow cytometry for cell viability, chemosensitivity, and apoptosis assessment.
  • RNA immunoprecipitation and dual-luciferase reporter assays to confirm molecular interactions.

Main Results:

  • TINCR and ERK-2 expression were upregulated, while miR-19b-3p was downregulated in DDP-resistant CM tissues and cells.
  • TINCR knockdown sensitized CM cells to DDP, reduced viability, and increased apoptosis.
  • TINCR directly targets miR-19b-3p, which in turn targets ERK-2, forming the TINCR/miR-19b-3p/ERK-2/NF-kb axis that drives DDP resistance.

Conclusions:

  • TINCR plays a crucial role in conferring DDP resistance in CM.
  • The TINCR/miR-19b-3p/ERK-2/NF-kb pathway is a key mechanism mediating DDP resistance in CM.
  • TINCR is a promising therapeutic target for overcoming DDP resistance in CM.
Keywords:
ERK-2TINCRchoroidal melanomacisplatinmiR-19b-3p

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