Asma Saeed
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Asma Saeed has a total of 9 co-authors. Here are the top co-authors by number of shared publications:
- Assaad Antoine Eid
Department of Anatomy, Cell Biology and Physiological Sciences, Faculty of Medicine, American University of Beirut, Beirut, Lebanon
1 shared publication - Borbala Mifsud
College of Health and Life Sciences, Hamad Bin Khalifa University, Doha P.O. Box 34110, Qatar
1 shared publication - Georges Nemer
College of Health and Life Sciences, Hamad Bin Khalifa University, Doha P.O. Box 34110, Qatar
1 shared publication - Jamila Hijazi
Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Beirut P.O. Box 110236, Lebanon
1 shared publication - Johan Ericsson
College of Health and Life Sciences, Hamad Bin Khalifa University, Doha P.O. Box 34110, Qatar
1 shared publication - Maria Teresa Bengoechea-Alonso
College of Health and Life Sciences, Hamad Bin Khalifa University, Doha P.O. Box 34110, Qatar
1 shared publication
Latest Publications
- Open Access
- 17 July 2026
- Published by MDPI AG in Current Issues in Molecular Biology
- Vol. 48 (7) , 731
p53 and p21 Status Influences Cellular Response to Metformin in KRAS-Mutant HCT116 Colorectal Cancer Cells
Colorectal cancer (CRC) remains a leading cause of cancer morbidity worldwide, highlighting the need for improved therapies. Metformin, a widely used antihyperglycemic agent, has gained attention for its potential antitumor properties. In this study, we evaluated the effects of the tumor suppressor genes TP53 and CDKN1A on metformin responsiveness in a KRAS-mutant CRC in vitro model using HCT116 cells harboring a G13D mutation in KRAS. Using parental (p53+/+, p21+/+) and isogenic knockout cell lines, we assessed cell-cycle distribution and transcriptomic responses following metformin treatment. In parental wild-type cells, metformin exposure was associated with a dose- and time-dependent reduction in cell viability and an increased proportion of cells in the G0/G1 phase, with significance levels across treatment conditions ranging from p = 0.03 to p < 0.0001. Loss of p53 or p21 was associated with attenuated cellular responses to metformin, with p21-deficient cells responding primarily at higher doses and prolonged exposure (72 h). Transcriptomic profiling revealed extensive differential gene expression in parental cells (1399 DEGs), compared with more limited responses in p53−/− (270 DEGs) and p21−/− cells (32 DEGs). Differentially expressed genes associated with MAPK signaling (DUSP5) and inflammatory regulation (TNFAIP3) were observed across genotypes, whereas pathway enrichment of DNA replication and chromatin organization was specific to p53-deficient cells. These findings provide a transcriptomic and phenotypic characterization of genotype-dependent cellular responses to metformin and establish a basis for future mechanistic and functional validation studies.
- 17 July 2026
- Published by MDPI AG in Current Issues in Molecular Biology
- Vol. 48 (7) , 731
Open Accessp53 and p21 Status Influences Cellular Response to Metformin in KRAS-Mutant HCT116 Colorectal Cancer Cells
Colorectal cancer (CRC) remains a leading cause of cancer morbidity worldwide, highlighting the need for improved therapies. Metformin, a widely used antihyperglycemic agent, has gained attention for its potential antitumor properties. In this study, we evaluated the effects of the tumor suppressor genes TP53 and CDKN1A on metformin responsiveness in a KRAS-mutant CRC in vitro model using HCT116 cells harboring a G13D mutation in KRAS. Using parental (p53+/+, p21+/+) and isogenic knockout cell lines, we assessed cell-cycle distribution and transcriptomic responses following metformin treatment. In parental wild-type cells, metformin exposure was associated with a dose- and time-dependent reduction in cell viability and an increased proportion of cells in the G0/G1 phase, with significance levels across treatment conditions ranging from p = 0.03 to p < 0.0001. Loss of p53 or p21 was associated with attenuated cellular responses to metformin, with p21-deficient cells responding primarily at higher doses and prolonged exposure (72 h). Transcriptomic profiling revealed extensive differential gene expression in parental cells (1399 DEGs), compared with more limited responses in p53−/− (270 DEGs) and p21−/− cells (32 DEGs). Differentially expressed genes associated with MAPK signaling (DUSP5) and inflammatory regulation (TNFAIP3) were observed across genotypes, whereas pathway enrichment of DNA replication and chromatin organization was specific to p53-deficient cells. These findings provide a transcriptomic and phenotypic characterization of genotype-dependent cellular responses to metformin and establish a basis for future mechanistic and functional validation studies.