SRSF3 Restriction Eases Cervical Cancer Cell Viability and Metastasis via Adjusting PI3K/AKT/mTOR Signaling Pathway

Lirong Zhang1, Jing Li1, Liping Zhang1

  • 1Department of Gynecology, Wuhan Childrens Hospital, Wuhan Maternal and Child Health Hospital, Wuhan Womens and Childrens Health Care Center, Wuhan, Hubei Province, China.

Abstract

Insights

Reducing SRSF3 levels inhibits cervical cancer cell viability and metastasis. This occurs by suppressing the PI3K/AKT/mTOR signaling pathway, offering a potential therapeutic target for cervical cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Cervical cancer (CC) remains a significant global health concern.
  • Understanding the molecular mechanisms driving CC progression is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the role of SRSF3 in the viability and metastasis of cervical cancer (CC) cell lines (SiHa and HeLa).
  • To elucidate the impact of SRSF3 modulation on the PI3K/AKT/mTOR signaling pathway.

Main Methods:

  • In vitro culture of HeLa and SiHa cervical cancer cells.
  • RNA interference (RNAi) to reduce SRSF3 expression, confirmed by RT-PCR.
  • Cell Counting Kit-8 (CCK-8) assay to assess cell viability.
  • Transwell assays to evaluate cell migration and invasion.
  • Western blotting to analyze protein levels in the PI3K/AKT/mTOR pathway.

Main Results:

  • Downregulation of SRSF3 significantly reduced cell viability and invasion in both SiHa and HeLa cells in a time-dependent manner.
  • SRSF3 reduction led to decreased phosphorylation of key proteins in the PI3K/AKT/mTOR pathway (p-PI3K/PI3K, p-AKT/AKT, p-mTOR/mTOR).
  • Viability effects were observed starting at 48 hours post-treatment, with no significant difference at 24 hours.

Conclusions:

  • SRSF3 plays a critical role in promoting cervical cancer cell viability and metastasis.
  • Inhibition of SRSF3 effectively suppresses CC progression by downregulating the PI3K/AKT/mTOR signaling pathway.
  • Targeting SRSF3 presents a promising therapeutic strategy for cervical cancer.

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