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Mechanism of lncRNA SNHG16 on kidney clear cell carcinoma cells by targeting miR-506-3p/ETS1/RAS/ERK molecular axis

Tao Cheng1, Ming-Li Gu1, Wei-Qiang Xu1

  • 1Department of Urology, The Second Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui, 233000, China.

Heliyon
|May 17, 2024
PubMed
Abstract

Insights

Long noncoding RNA SNHG16 promotes kidney cancer progression by targeting miR-506-3p, ETS1, and the RAS/ERK pathway. This finding offers insights into kidney clear cell carcinoma (KIRC) diagnosis and treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Kidney clear cell carcinoma (KIRC) is a prevalent malignancy with complex molecular underpinnings.
  • Understanding the regulatory mechanisms of KIRC is crucial for developing effective therapeutic strategies.

Purpose of the Study:

  • To elucidate the role of long noncoding RNA SNHG16 in KIRC.
  • To investigate the molecular axis involving SNHG16, miR-506-3p, ETS1, and the RAS/ERK pathway in KIRC pathogenesis.

Main Methods:

  • Analysis of SNHG16, miR-506-3p, ETS1, RAS, and ERK expression in KIRC tissues and adjacent normal tissues.
  • In vitro experiments involving transfection of KIRC cells with overexpressed or silenced SNHG16.
  • Rescue experiments to validate the molecular interactions and pathway activation.

Main Results:

  • SNHG16 and ETS1 were upregulated, while miR-506-3p was downregulated in KIRC tissues, correlating with activated RAS/ERK signaling.
  • SNHG16 knockdown inhibited KIRC cell proliferation, invasion, and migration while promoting apoptosis.
  • Rescue experiments confirmed SNHG16's oncogenic role via the miR-506-3p/ETS1/RAS/ERK axis.

Conclusions:

  • Long noncoding RNA SNHG16 promotes KIRC progression by targeting the miR-506-3p/ETS1/RAS/ERK molecular axis.
  • The SNHG16/miR-506-3p/ETS1/RAS/ERK pathway represents a potential therapeutic target for KIRC.
Keywords:
ETS1Kidney clear cell carcinomaProliferation and migrationRAS/ERK signaling pathwaylncRNA SNHG16miR-506-3p

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