Hsa_circRNA_101036 aggravates hypoxic-induced endoplasmic reticulum stress via the miR-21-3p/TMTC1 axis in oral squamous cell carcinoma

  • 0Department of Oral and Maxillofacial Surgery, Hainan General Hospital (Hainan Affiliated Hospital of Hainan Medical University), Haikou, China.

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Summary

This summary is machine-generated.

Hsa_circRNA_101036 acts as a tumor suppressor in oral squamous cell carcinoma (OSCC) by inducing endoplasmic reticulum stress and apoptosis. It regulates TMTC2 expression via sponging miR-21-3p, offering a potential therapeutic target for OSCC.

Area Of Science

  • Molecular Biology
  • Oncology
  • Biochemistry

Background

  • Circular RNAs (circRNAs) are emerging as critical regulators in cancer, including oral squamous cell carcinoma (OSCC).
  • Hsa_circRNA_101036 has been identified as a potential tumor suppressor in OSCC, but its regulatory mechanisms require elucidation.
  • Understanding the role of hsa_circRNA_101036 is crucial for developing novel therapeutic strategies against OSCC.

Purpose Of The Study

  • To investigate the regulatory mechanism of hsa_circRNA_101036 in the development and progression of OSCC.
  • To explore the potential of hsa_circRNA_101036 as a therapeutic target for OSCC.
  • To elucidate the interaction between hsa_circRNA_101036, miR-21-3p, and TMTC2 in OSCC under hypoxic conditions.

Main Methods

  • Bioinformatic analysis using StarBase v.2.0 to predict miRNA targets.
  • Quantitative assessment of hsa_circRNA_101036, miR-21-3p, and TMTC2 expression in OSCC tissues and cell lines.
  • Functional assays including cell viability, migration, invasion, apoptosis, and reactive oxygen species (ROS) analysis following hsa_circRNA_101036 overexpression under hypoxic conditions.

Main Results

  • Hsa_circRNA_101036 and TMTC2 expression were downregulated, while miR-21-3p was upregulated in OSCC tissues compared to adjacent tissues.
  • Hypoxia significantly decreased hsa_circRNA_101036 and TMTC2 expression while increasing miR-21-3p, HIF-1α, ER stress markers, apoptosis, and ROS levels.
  • Overexpression of hsa_circRNA_101036 suppressed tumor growth, induced ER stress, apoptosis, and ROS production, and upregulated TMTC2 by sponging miR-21-3p.

Conclusions

  • Hsa_circRNA_101036 functions as a crucial tumor suppressor in OSCC development and progression.
  • Hsa_circRNA_101036 exacerbates ER stress, apoptosis, and ROS production in OSCC cells under hypoxic conditions.
  • Hsa_circRNA_101036 upregulates TMTC2 by sponging miR-21-3p, highlighting a novel regulatory axis in OSCC.

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