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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.
Objective:
To investigate the effect of SRSF3 on the viability and metastasis of cervical cancer (CC) SiHa and Hela cells.
Methods:
In vitro, HeLa cells and SiHa cells were cultured. In cervical cancer cells, RNA interference technology was utilized to lessen the SRSF3 level, and via RT-PCR utilization, the SRSF3 level in every group of cells was revealed. By employing the CCK-8 method, the OD value was revealed in every group at 24, 48, 72, and 96 h. On the migration of cervical cancer SiHa and HeLa cells via transwell utilizing, the consequence of SRSF3 was surveyed. Through western blotting utilizing, the PI3K/AKT/mTOR signaling pathway-connected proteins levels was revealed.
Results:
In SiHa cells, contrasted to the NC-SiHa group, the SRSF3 level, the number of invasive cells per unit area, the p-PI3K/PI3K level, the p-AKT/AKT level, and the p-mTOR/mTOR level in the si-SRSF3 group were substantially lessened. The OD value at 490 nm of the si-SRSF3 group had no impressive divergence, contrasted to the NC-SiHa group at 24 h. At 48 h, the OD value of the si-SRSF3 group was impressively lessened than that of the NC-SiHa group. This connection was time-dependent. In HeLa cells, the SRSF3 level, the number of invasive cells per unit area, the level of p-PI3K/PI3K, the level of p-AKT/AKT, and the level of p-mTOR/mTOR in the cells of the si-SRSF3 group in the NC-HeLa group were impressively lessened than those in the NC-Hela group. Between the NC-HeLa group and the si-SRSF3 group at 24 h, there was no impressive divergence in the OD value at 490 nm. At 48 h, the OD value of the si-SRSF3 group was impressively lessened than that of the NC-SiHa group. This connection is time-dependent.
Conclusion:
Reducing the SRSF3 level can restrain the viability and metastasis of cervical cancer cells via restraining the PI3K/AKT/mTOR signaling pathway.
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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