mGluR5 promotes the progression of multiple myeloma in vitro via Ras-MAPK signaling pathway

Adv Clin Exp Med. 2022 Aug;31(8):881-888. doi: 10.17219/acem/130445.

Abstract

Background: Multiple myeloma (MM) is a malignant plasma cancer which remains difficult to be cured. Recently, numerous research studies have appeared, exploring MM from molecular level. However, there is no study about the impact of metabotropic glutamate receptors (mGluRs), especially mGluR5, on MM progression. Thus, the present research was dedicated to the exploration of the influence of mGluR5 on MM.

Objectives: In this research, we used quantitative real-time polymerase chain reaction (qRT-PCR) to check the gene expression in MM, western blot assay to check the protein expression of the gene, MTT assay to quantify the cell viability, and flow cytometry (FCM) apoptosis method to evaluate cell apoptosis in order to acquire the results. The purpose was to assess the role of mGluR5 in MM cells.

Material and methods: The qRT-PCR was used and it was found that mGluR5 was overexpressed in MM cell lines and MM tissues compared to normal ones. To better observe the function of mGluR5 in MM, cell viability and apoptosis were checked using MTT and FCM apoptosis assays after the treatment with agonists and antagonists.

Results: Agonist-induced mGluR5 upregulation could promote MM cell viability and inhibit apoptosis. The same results were obtained through MTT and FCM apoptosis assays after upregulation and downregulation of mGluR5 by transfection. To further investigate the inner mechanism, the effect of mGluR5 on Ras-MAPK pathway was checked using western blot. It was found that the upregulation of mGluR5 could activate the Ras-MAPK pathway.

Conclusions: The mGluR5 might be involved in promoting cell proliferation and inhibiting cell apoptosis in MM. It can be an essential biomarker in the screening for MM and a potential part of future MM therapies.

Keywords: apoptosis; mGluR5; multiple myeloma; viability.

MeSH terms

  • Apoptosis
  • Cell Line, Tumor
  • Cell Proliferation
  • Down-Regulation
  • Humans
  • MAP Kinase Signaling System
  • Multiple Myeloma* / drug therapy
  • Receptor, Metabotropic Glutamate 5 / metabolism*
  • Signal Transduction
  • ras Proteins / metabolism

Substances

  • Receptor, Metabotropic Glutamate 5
  • ras Proteins