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Updated: Jul 9, 2025

Utilizing Functional Genomics Screening to Identify Potentially Novel Drug Targets in Cancer Cell Spheroid Cultures
Published on: December 26, 2016
Targeted down-regulation of SRSF1 exerts anti-cancer activity in OSCC through impairing lysosomal function and
Yi Qu1, Ying He1, Yijuan Wang2
1Department of Oral and Maxillofacial & Head and Neck Oncology, Beijing Stomatological Hospital, Capital Medical University, Beijing 100050, China.
Abstract:
Oral squamous cell carcinoma (OSCC) is a common cancer of the head and neck. Despite ongoing efforts, there remains a dearth of targeted drugs capable of effectively inhibiting OSCC growth. As the earliest discovered proto-oncogene in the SRSF family, targeted inhibition of serine/arginine-rich splicing factor 1 (SRSF1) plays an important role in tumor suppression. However, the expression, function, and mechanism of SRSF1 in OSCC have not been comprehensively reported. This study retrospectively analyzed clinical samples from OSCC patients and discovered a significant correlation between the SRSF1 expression level and poor prognosis. In vitro experimentation demonstrated that SRSF1 knockdown inhibited OSCC growth, survival, lysosomal biogenesis and autophagy. To confirm the significance of lysosomal function and autophagy in the regulation of OSCC growth by SRSF1, cell rescue models were constructed. The aforementioned findings were subsequently validated in xenograft models. Ultimately, targeted knockdown of SRSF1 was found to significantly suppress OSCC growth by impeding lysosomal biogenesis and autophagy.
Insights
Targeting serine/arginine-rich splicing factor 1 (SRSF1) inhibits oral squamous cell carcinoma (OSCC) growth. This study reveals SRSF1 knockdown impedes tumor progression by disrupting lysosomal biogenesis and autophagy.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Oral squamous cell carcinoma (OSCC) is a prevalent head and neck cancer with limited targeted therapies.
- Serine/arginine-rich splicing factor 1 (SRSF1), a proto-oncogene, is implicated in tumor suppression, but its role in OSCC is unclear.
Purpose of the Study:
- To investigate the expression, function, and mechanism of SRSF1 in OSCC.
- To determine the prognostic significance of SRSF1 in OSCC patients.
- To evaluate SRSF1 as a potential therapeutic target for OSCC.
Main Methods:
- Retrospective analysis of clinical OSCC samples.
- In vitro experiments involving SRSF1 knockdown in OSCC cell lines.
- Construction of cell rescue models to assess lysosomal and autophagy pathways.
- In vivo validation using xenograft models.
Main Results:
- Elevated SRSF1 expression correlates with poor prognosis in OSCC patients.
- SRSF1 knockdown significantly inhibits OSCC cell growth, survival, lysosomal biogenesis, and autophagy.
- Targeted SRSF1 inhibition suppresses OSCC growth in xenograft models by affecting these pathways.
Conclusions:
- SRSF1 plays a critical role in OSCC progression.
- Targeting SRSF1 represents a promising therapeutic strategy for OSCC.
- Inhibition of SRSF1 suppresses OSCC by disrupting lysosomal biogenesis and autophagy.
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