Silencing SOX2OT reduces viability and migration in lung cancer cells via lncRNA and protein regulation
Mohadeseh Zarei1, Ali Dinari2, Babak Jahangiri1
1Department of Molecular Medicine, Institute of Medical Biotechnology, National Institute of Genetic Engineering and Biotechnology (NIGEB), Tehran, Iran.
Abstract:
Long non-coding RNAs (lncRNAs) play crucial role in tumor development and are being explored as potential therapeutic targets in lung cancer. Both SOX2OT and SOX2 are consistently overexpressed in lung cancer, suggesting that SOX2OT may play a significant role in its development. This study examines how knocking down SOX2OT affects the expression of specific lncRNAs (LINC00982, LINC00668, SNHG7), the gene P16, and key cell cycle-regulating proteins (HSP90AA1, EP300, YES1) in lung cancer cells. Silencing of SOX2OT in A549 and Calu-3 cells led to a marked reduction in its expression. This downregulation was accompanied by decreased levels of SNHG7 and LINC00668, while LINC00982 and P16 transcripts were strongly induced. At the protein level, EP300, HSP90AA1, and YES1 were substantially reduced, whereas P16 was notably elevated. Functionally, suppression of SOX2OT impaired cell viability and significantly limited migratory capacity. In parallel, apoptosis assays demonstrated a pronounced increase in apoptotic cell populations following SOX2OT knockdown. SOX2OT regulates specific lncRNAs and proteins involved in lung cancer survival and migration. Silencing SOX2OT significantly reduces viability, migration, and survival of lung cancer cells, suggesting its potential as a therapeutic target. Further in vivo validation and rescue experiments are needed to confirm these mechanisms.
Insights
Silencing SOX2OT, a long non-coding RNA, significantly reduces lung cancer cell viability and migration. This suggests SOX2OT is a potential therapeutic target for lung cancer treatment.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- Long non-coding RNAs (lncRNAs) are implicated in tumor development and are emerging as therapeutic targets in lung cancer.
- SOX2OT is overexpressed in lung cancer, indicating its potential role in tumorigenesis.
Purpose of the Study:
- To investigate the functional role of SOX2OT in lung cancer.
- To determine the effects of SOX2OT knockdown on specific lncRNAs, gene expression, and protein levels in lung cancer cells.
Main Methods:
- SOX2OT was silenced in A549 and Calu-3 lung cancer cell lines.
- Expression levels of lncRNAs (LINC00982, LINC00668, SNHG7), P16 gene, and proteins (HSP90AA1, EP300, YES1) were analyzed.
- Cell viability, migration, and apoptosis assays were performed.
Main Results:
- SOX2OT silencing decreased SNHG7 and LINC00668 expression, while increasing LINC00982 and P16.
- Protein levels of EP300, HSP90AA1, and YES1 were reduced, and P16 was elevated.
- Suppression of SOX2OT impaired cell viability, reduced migration, and increased apoptosis.
Conclusions:
- SOX2OT regulates key lncRNAs and proteins involved in lung cancer cell survival and migration.
- Silencing SOX2OT demonstrates therapeutic potential by reducing lung cancer cell viability and migration.
- Further in vivo studies are warranted to validate these findings and explore therapeutic strategies.
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