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The potential role of SNHG16/ miRNA-146a/ TRAF6 signaling pathway in the protective effect of zoledronate against colorectal cancer and associated osteoporosis in mouse model

  • 0Department of Clinical Pharmacology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
International Immunopharmacology +

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April 24, 2024

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April 24, 2024

View abstract on PubMed

Summary

This summary is machine-generated.

Zoledronate (ZOL) may prevent colorectal cancer (CRC) and osteoporosis (OP) by modulating the SNHG16/miRNA-146a/TRAF6 pathway. This study shows ZOL improves bone density and reduces cancer markers in a mouse model.

Area Of Science

  • Oncology
  • Orthopedics
  • Molecular Biology

Background

  • Colorectal cancer (CRC) with associated osteoporosis (OP) increases mortality.
  • The SNHG16/miRNA-146a/TRAF6 pathway drives cancer progression and metastasis.

Purpose Of The Study

  • To investigate the effect of zoledronate (ZOL) on CRC and associated OP in a mouse model.
  • To analyze the modulation of the SNHG16/miRNA-146a/TRAF6 pathway by ZOL.

Main Methods

  • A mouse model using azoxymethane (AOM)/dextran sodium sulfate (DSS) was established.
  • Mice were treated with ZOL, and body weight, gene expression (SNHG16, miRNA-146a, TRAF6), and histopathology were analyzed.
  • Immunohistochemistry for CK20, pKi-67, CDx2, RANK, and OPG, along with CT scans, were performed.

Main Results

  • ZOL significantly decreased SNHG16 and TRAF6 expression while increasing miRNA-146a in the colon and bone.
  • ZOL improved colon histopathology, reduced CK20 and Ki-67, and increased CDx2 expression.
  • ZOL prevented osteoporotic changes, reduced RANK, increased OPG, and improved bone mineral density.

Conclusions

  • Zoledronate shows promise as a preventive therapy for colitis-induced cancer and associated osteoporosis.
  • ZOL exerts its effects through modulation of the SNHG16, miRNA-146a, and TRAF6 signaling pathway.

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