Cytotoxic effects and expressional modifications by sericin in liver cancer cells
Year: 2025
Type: article
Abstract: Background: Liver cancer is the 3rd leading cause of cancer related deaths worldwide with increased risk in males than females. Many natural derivatives are being used as anticancer agents due to their antioxidant and cytotoxic potential. Silk sericin, extracted by the degumming of silkworm cocoon, has emerged as a novel potential anticancer compound. Due to increased elasticity, stability and ease of access made it an important protein for research in cancer studies. In this study, cytotoxic effects of sericin and its impact on expressional changes of selected genes in liver cancer cells were investigated. Methods: Cultured HepG2 cells were treated with extracted sericin by the degumming of local cocoons and commercially available purified sericin (0.03-1 mg/ml) for 24-72 hours. MTT dye reduction assay was used to determine the inhibitory effects of sericin on cultured HepG2 cells. Expressional analysis of GADD45A, GADD45B and CDKN1A was done by real-time PCR. Fold changes were determined by Livak method while comparing the results with untreated controls. Results: The cytotoxic effect of sericin (pure and extracted) was concentration dependent as seen by increasing concentration, the suppression of proliferation became more pronounced. The effects were more intense after the mid-interval exposure period (48 hour). GADD45A was inhibited moderately whereas GADD45B and CDKN1A were induced with increasing concentration of sericin. Conclusion: Proliferation of HepG2 cells was inhibited by sericin exposure. Sericin also showed potential to regulate the expression of genes involved in DNA repair, cell cycle progression, DNA damage and apoptosis.
Source: Biomedical Current Insights
DOI: 10.63626/zrb7jf61
Authors: Umm-E-Ammarah Mehak, Zainab Quratulain Azher, Sana Iqbal
Language: English
Subfield: Biomaterials
Field: Materials Science
Domain: Physical Sciences
Open Access status: hybrid
OpenAlex ID: W4412181185
