Parathyroid hormone type 1 receptor regulates osteosarcoma K7M2 Cell growth by interacting with angiotensinogen

Shenglong Li1, Fei Liu1, Yi Pei1

  • 1Department of Bone and Soft Tissue Tumor Surgery, Liaoning Cancer Hospital & Institute, Cancer Hospital of China Medical University, Shenyang, China.

Insights

Parathyroid hormone type 1 receptor (PTHR1) interference impacts osteosarcoma (OS) cell growth and spread. PTHR1 affects OS cell viability, apoptosis, and migration, potentially by regulating angiotensinogen (AGT) and chemokine ligand 9 (CCL9).

Area of Science:

  • Oncology
  • Molecular Biology
  • Endocrinology

Background:

  • Osteosarcoma (OS) is a primary bone malignancy with limited treatment options.
  • The parathyroid hormone type 1 receptor (PTHR1) and angiotensinogen (AGT) pathways are implicated in various cellular processes, but their interplay in OS is not fully understood.

Purpose of the Study:

  • To investigate the interaction between PTHR1 and AGT in osteosarcoma cells.
  • To elucidate the effects of modulating PTHR1 and AGT on OS cell behavior, including viability, apoptosis, migration, invasion, and cell cycle progression.

Main Methods:

  • A stably transfected mouse OS cell line (shPTHR1-K7M2) was generated using shRNA to knock down PTHR1.
  • siRNA was used to knock down AGT expression.
  • Real-time quantitative PCR, Cell Counting Kit-8, crystal violet staining, flow cytometry, and Transwell assays were employed to assess gene expression and cellular functions.

Main Results:

  • PTHR1 interference upregulated AGT and CCR3 expression while downregulating CCL9.
  • Knockdown of PTHR1 significantly decreased OS cell viability, migration, invasion, and colony formation, and increased apoptosis.
  • AGT knockdown further inhibited cell viability but promoted migration and invasion in PTHR1-interfered cells.

Conclusions:

  • PTHR1 plays a crucial role in regulating osteosarcoma cell proliferation, apoptosis, migration, and invasion.
  • The observed effects of PTHR1 interference are potentially mediated through the regulation of the AGT/CCL9 signaling axis.

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