BCSG1 siRNA delivered by lentiviral vector suppressed proliferation and migration of MDA-MB-231 cells

Jin-Song He1, Ni Xie2, Jian-Bo Yang3

  • 1Department of Breast Surgery, Peking University Shenzhen Hospital, Shenzhen, Guangdong 518035, P.R. China.

Insights

Breast cancer-specific gene 1 (BCSG1) siRNA delivered via lentiviral vector effectively reduced BCSG1 expression in breast cancer cells. This suppression inhibited cell migration and proliferation, potentially by lowering p-AKT and p-ERK protein levels.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Therapy

Background:

  • Breast cancer-specific gene 1 (BCSG1), also known as γ-synuclein (SNCG), is overexpressed in invasive breast carcinomas.
  • BCSG1 is notably absent in normal and benign breast tissues, suggesting its role in breast cancer progression.

Purpose of the Study:

  • To investigate the therapeutic potential of BCSG1 siRNA delivered by lentiviral vectors in breast cancer cells.
  • To elucidate the underlying molecular mechanisms by which BCSG1 affects cancer cell behavior.

Main Methods:

  • Construction and transfection of a BCSG1 RNAi lentiviral vector into MDA-MB-231 breast cancer cells.
  • Quantification of BCSG1 mRNA levels using quantitative polymerase chain reaction (qPCR).
  • Assessment of cell proliferation (Cell Counting Kit-8), migration (Transwell assay), apoptosis (flow cytometry), and protein expression (Western blotting for AKT, ERK, p-AKT, p-ERK).

Main Results:

  • BCSG1 siRNA significantly reduced BCSG1 mRNA levels in MDA-MB-231 cells.
  • A notable decrease in cell migration and proliferation was observed, along with cell cycle arrest.
  • Western blot analysis revealed significantly lower levels of phosphorylated AKT (p-AKT) and phosphorylated ERK (p-ERK) in BCSG1 siRNA-treated cells.

Conclusions:

  • Lentiviral vector-mediated delivery of BCSG1 siRNA effectively suppresses BCSG1 expression in breast cancer cells.
  • BCSG1 siRNA treatment inhibits cancer cell migration and proliferation.
  • The observed effects are potentially mediated through the downregulation of p-AKT and p-ERK signaling pathways.

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