Nikhil Prasad Fact checked by:Thailand Medical News Team Feb 25, 2026 2 hours, 7 minutes ago
Medical News: Oral cancer continues to pose a major global health challenge, with oral squamous cell carcinoma, or OSCC, being the most common and aggressive form. Now, new laboratory research suggests that a natural plant compound found in parsley, celery, and chamomile may selectively weaken oral cancer cells while leaving healthy gum cells largely unharmed.
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Natural plant compound selectively disrupts oral cancer cell survival while protecting normal gum tissue
Researchers from the Interdisciplinary Center for Dental Research and Development at “Carol Davila” University of Medicine and Pharmacy in Bucharest, the Department of Biochemistry and Molecular Biology at the University of Bucharest, multiple departments within the Faculty of Dental Medicine at “Carol Davila” University, and the Department of Biochemistry and Molecular Biology at the Faculty of Pharmacy, University of Complutense of Madrid, Spain, conducted a detailed investigation into how apigenin affects normal and cancerous oral cells.
Why Oral Cancer Is So Difficult to Treat
OSCC accounts for more than 90 percent of oral cancers and is known for its high recurrence rate, resistance to therapy, and ability to spread. Even with surgery, radiotherapy, and targeted drugs, five-year survival rates remain around 60 percent. Scientists are therefore searching for treatments that can attack cancer cells without damaging normal tissues.
This
Medical News report focuses on how apigenin may offer that type of selective action.
Comparing Healthy and Cancer Cells
The team studied two types of cells in the lab. One was normal human gingival epithelial cells derived from healthy gum tissue. The other was OECM-1 cells, a well-established model of oral squamous cell carcinoma originating from malignant gingival tissue.
Both cell types were exposed to apigenin at different concentrations for 24 and 48 hours. The scientists then measured cell growth, energy production, oxidative stress, antioxidant defenses, autophagy activity, and apoptosis-related proteins.
Healthy Cells Activate Protective Mechanisms
In healthy gum cells, apigenin did not show toxic effects. In fact, at higher concentrations, mitochondrial metabolic activity increased by about 20 percent after 24 hours. Although there was a moderate rise in reactive oxygen species, especially after 48 hours, these increases were controlled.
Importantly, levels of glutathione, a major antioxidant molecule, increased over time. This suggests that healthy cells activated their internal defense systems. Autophagy, the natural process by which cells recycle damaged components, also increased significantly by more than 50 percent. This indicates that healthy cells used autophagy as a protective survival mechanism under mild stress.
Energy levels showed only temporary changes. While ATP briefly decreased at 24 hours at higher doses, levels recovered by 48 hours, demonstrati
ng metabolic adaptability without permanent harm.
Cancer Cells Experience Severe Oxidative Stress
The response in oral cancer cells was strikingly different. Apigenin significantly reduced mitochondrial metabolic activity at both doses and time points. After 24 hours, ATP levels dropped by more than 30 percent compared to untreated cancer cells.
At the same time, reactive oxygen species surged dramatically. At the higher concentration, ROS levels increased up to 17-fold at 24 hours and remained elevated even at 48 hours. This indicates a severe oxidative imbalance inside the cancer cells.
Although ATP levels rebounded strongly at 48 hours, increasing several fold, this appeared to reflect a metabolic shift toward glycolysis rather than true recovery. The cancer cells likely switched energy production methods in an attempt to survive oxidative stress.
Autophagy Is Suppressed in Tumor Cells
While healthy cells increased autophagy, cancer cells showed the opposite effect. Autophagic activity decreased by up to 16 percent after treatment. This suggests that apigenin interfered with one of the cancer cells’ survival strategies.
On a molecular level, healthy cells showed reduced AKT signaling and moderate activation of caspases involved in controlled cell death. In contrast, cancer cells displayed increased anti-apoptotic signaling proteins and decreased stress-related JNK activation, indicating attempts to resist cell death despite the oxidative pressure.
What The Findings Mean
The most important takeaway from the study is that apigenin triggered fundamentally different biological responses depending on whether the cells were healthy or cancerous. Healthy gum cells managed oxidative stress through coordinated antioxidant and autophagy responses, maintaining structural integrity and viability. In contrast, oral cancer cells experienced redox imbalance, metabolic disruption, suppressed autophagy, and incomplete activation of cell death pathways.
The conclusions strongly suggest that apigenin exposes specific vulnerabilities in oral cancer cells linked to oxidative stress and redox signaling. By pushing tumor cells into metabolic and oxidative overload while sparing normal tissue, apigenin may serve as a promising adjunct agent in future OSCC treatment strategies. Its ability to create selective stress in malignant cells without widespread toxicity offers a potential pathway toward safer combination therapies that enhance cancer cell sensitivity to existing treatments.
The study findings were published in the peer reviewed International Journal of Molecular Sciences.
https://www.mdpi.com/1422-0067/27/5/2091
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Medical News.
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https://www.thailandmedical.news/articles/cancer
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