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| Format: | Recurso digital |
| Language: | English |
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2026
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| Online Access: | https://doi.org/10.5281/zenodo.18480497 |
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| author | Ali Alrasheed1*, Ahad Alwagdani2, Hadi Alaedh3, Sarah Alotaibi4, Hani Alharbi5, Amal Al-Zayed6, Faten Hakami7, Neamah Kinani8, Ayman A. Bawazeer9, Maher M Albalawi10, Nada Hakami11, Hadeel Alharbi12, Ghadeer Alasmari13, Yasir Alhassan14, Wedad Abohaddash15, Shouq Albalawi16 |
| author_facet | Ali Alrasheed1*, Ahad Alwagdani2, Hadi Alaedh3, Sarah Alotaibi4, Hani Alharbi5, Amal Al-Zayed6, Faten Hakami7, Neamah Kinani8, Ayman A. Bawazeer9, Maher M Albalawi10, Nada Hakami11, Hadeel Alharbi12, Ghadeer Alasmari13, Yasir Alhassan14, Wedad Abohaddash15, Shouq Albalawi16 |
| contents | <p><strong><span>Background:</span></strong><span> Liver cancer remains a major clinical challenge due to its aggressive progression and resistance to conventional therapies. The JAK-STAT signaling pathway and PD-1/PD-L1 immune checkpoint axis are key contributors to tumor growth and immune evasion. <strong>Objective:</strong> This study aimed to evaluate the combined therapeutic effect of Selenium Cysteine (SeCys) and 5-Fluorouracil (5-FU) on tumor growth inhibition, immune modulation, and signaling pathway regulation in a preclinical liver cancer model. <strong>Methods:</strong> We conducted an in vivo study with 250 subjects assigned to control, SeCys, 5-FU, or combination treatment groups. Tumor volumes, survival times, JAK-STAT pathway activation (pJAK2, pSTAT3), PD-L1 expression, and immune cell infiltration (CD8⁺ T-cells) were measured. Statistical analyses included ANOVA, Kruskal–Wallis tests, t-tests, Mann–Whitney U tests, and Pearson correlation. <strong>Results:</strong> Combination therapy significantly inhibited tumor growth (mean TGI 50.82%, p < 0.0001), reduced pSTAT3 levels (χ² = 88.456, p < 0.0001), and increased PD-L1 mRNA expression (t = 8.399, p < 0.0001) compared to controls. </span></p> |
| format | Recurso digital |
| id | zenodo_https___doi_org_10_5281_zenodo_18480497 |
| institution | Zenodo |
| language | eng |
| publishDate | 2026 |
| publisher | Zenodo |
| record_format | zenodo |
| spellingShingle | SYNERGISTIC SUPPRESSION OF TUMOR GROWTH BY SELENOCYSTINE AND 5-FLUOROURACIL THROUGH JAK/STAT PATHWAY INHIBITION AND IMMUNE CHECKPOINT REGULATION Ali Alrasheed1*, Ahad Alwagdani2, Hadi Alaedh3, Sarah Alotaibi4, Hani Alharbi5, Amal Al-Zayed6, Faten Hakami7, Neamah Kinani8, Ayman A. Bawazeer9, Maher M Albalawi10, Nada Hakami11, Hadeel Alharbi12, Ghadeer Alasmari13, Yasir Alhassan14, Wedad Abohaddash15, Shouq Albalawi16 <p><strong><span>Background:</span></strong><span> Liver cancer remains a major clinical challenge due to its aggressive progression and resistance to conventional therapies. The JAK-STAT signaling pathway and PD-1/PD-L1 immune checkpoint axis are key contributors to tumor growth and immune evasion. <strong>Objective:</strong> This study aimed to evaluate the combined therapeutic effect of Selenium Cysteine (SeCys) and 5-Fluorouracil (5-FU) on tumor growth inhibition, immune modulation, and signaling pathway regulation in a preclinical liver cancer model. <strong>Methods:</strong> We conducted an in vivo study with 250 subjects assigned to control, SeCys, 5-FU, or combination treatment groups. Tumor volumes, survival times, JAK-STAT pathway activation (pJAK2, pSTAT3), PD-L1 expression, and immune cell infiltration (CD8⁺ T-cells) were measured. Statistical analyses included ANOVA, Kruskal–Wallis tests, t-tests, Mann–Whitney U tests, and Pearson correlation. <strong>Results:</strong> Combination therapy significantly inhibited tumor growth (mean TGI 50.82%, p < 0.0001), reduced pSTAT3 levels (χ² = 88.456, p < 0.0001), and increased PD-L1 mRNA expression (t = 8.399, p < 0.0001) compared to controls. </span></p> |
| title | SYNERGISTIC SUPPRESSION OF TUMOR GROWTH BY SELENOCYSTINE AND 5-FLUOROURACIL THROUGH JAK/STAT PATHWAY INHIBITION AND IMMUNE CHECKPOINT REGULATION |
| url | https://doi.org/10.5281/zenodo.18480497 |