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Article Abstract
Background: Lung cancer, a lethal type of malignancy in the world, has different pathological subcategories, among which NSCLC is the most common form. The complex pathogenesis of this disease has caused its treatment in advanced stages to be accompanied by many problems. Recently, the genes involved in metabolism, especially those coding for membrane transporter proteins (the solute carrier) have received attention in cancer studies. The Solute Carrier Family 16 Member 1 (SLC16A) is membrane transporters the role of which in the promotion of cancer has been revealed in recent years. This study aimed to examine the effect of SLC16A13 low expression in A549 lung cancer cells, focusing on its role in key cellular processes such as viability, proliferation, and apoptosis. By targeting SLC16A13, a critical member of the solute carrier family implicated in cancer metabolism, the study search for to uncover molecular mechanisms that could inform novel therapeutic strategies for non-small cell lung cancer.
Methods: At first, the A549 lung cancer cell line was cultured in a standard medium, and then specific synthetic SLC16A13 sh-RNA was transfected into the A549 cell line to suppress the expression of this membrane transporter. We used MTT and flow cytometry tests to investigate the effect of reducing the expression of SLC16A13 on the process of cell viability and apoptosis. Also, the change of gene expression was analyzed by Real-Time PCR.
Results: In the present study, the reduction of SLC16A13 gene expression caused an increase in the apoptosis rate and reduced cell viability in lung cancer cells. Also, SLC16A13 suppression may induce apoptosis pathway by upregulating Bax, Caspase-3, and Caspase-9 expression while downregulation Bcl-2 expression. Besides, it was shown that SLC16A13 downregulation couldn't affect E-cadherin expression.
Conclusion: SLC16A13 may a promising target to increase cell death in lung cancer cells by inducing apoptosis pathways.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12118009 | PMC |
| http://dx.doi.org/10.31557/APJCP.2025.26.2.525 | DOI Listing |
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